Intelligent life on a planet comes of age when it first works out the reason for its own existence. If superior creatures from space ever visit earth, the first question they will ask, in order to assess the level of our civilization, is: ‘Have they discovered evolution yet?’ Living organisms had existed on earth, without ever knowing why, for over three thousand million years before the truth finally dawned on one of them. His name was Charles Darwin. To be fair, others had had inklings of the truth, but it was Darwin who first put together a coherent and tenable account of why we exist. Darwin made it possible for us to give a sensible answer to the curious child whose question heads this chapter. We no longer have to resort to superstition when faced with the deep problems: Is there a meaning to life? What are we for? What is man? After posing the last of these questions, the eminent zoologist G. G. Simpson put it thus: ‘The point I want to make now is that all attempts to answer that question before 1859 are worthless and that we will be better off if we ignore them completely’.*

Today the theory of evolution is about as much open to doubt as the theory that the earth goes round the sun, but the full implications of Darwin’s revolution have yet to be widely realized. Zoology is still a minority subject in universities, and even those who choose to study it often make their decision without appreciating its profound philosophical significance. Philosophy and the subjects known as ‘humanities’ are still taught almost as if Darwin had never lived. No doubt this will change in time. In any case, this book is not intended as a general advocacy of Darwinism. Instead, it will explore the consequences of the evolution theory for a particular issue. My purpose is to examine the biology of selfishness and altruism.

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Apart from its academic interest, the human importance of this subject is obvious. It touches every aspect of our social lives, our loving and hating, fighting and cooperating, giving and stealing, our greed and our generosity. These are claims that could have been made for Lorenz’s On Aggression, Ardrey’s The Social Contract, and Eibl-Eibesfeldt’s Love and Hate. The trouble with these books is that their authors got it totally and utterly wrong. They got it wrong because they misunderstood how evolution works. They made the erroneous assumption that the important thing in evolution is the good of the species (or the group) rather than the good of the individual (or the gene). It is ironic that Ashley Montagu should criticize Lorenz as a ‘direct descendant of the “nature red in tooth and claw” thinkers of the nineteenth century . . .’. As I understand Lorenz’s view of evolution, he would be very much at one with Montagu in rejecting the implications of Tennyson’s famous phrase. Unlike both of them, I think ‘nature red in tooth and claw’ sums up our modern understanding of natural selection admirably.

Before beginning on my argument itself, I want to explain briefly what sort of an argument it is, and what sort of an argument it is not. If we were told that a man had lived a long and prosperous life in the world of Chicago gangsters, we would be entitled to make some guesses as to the sort of man he was. We might expect that he would have qualities such as toughness, a quick trigger finger, and the ability to attract loyal friends. These would not be infallible deductions, but you can make some inferences about a man’s character if you know something about the conditions in which he has survived and prospered. The argument of this book is that we, and all other animals, are machines created by our genes. Like successful Chicago gangsters, our genes have survived, in some cases for millions of years, in a highly competitive world. This entitles us to expect certain qualities in our genes. I shall argue that a predominant quality to be expected in a successful gene is ruthless selfishness. This gene selfishness will usually give rise to selfishness in individual behaviour. However, as we shall see, there are special circumstances in which a gene can achieve its own selfish goals best by fostering a limited form of altruism at the level of individual animals. ‘Special’ and ‘limited’ are important words in the last sentence. Much as we might wish to believe otherwise, universal love and the welfare of the species as a whole are concepts that simply do not make evolutionary sense.

This brings me to the first point I want to make about what this book is not. I am not advocating a morality based on evolution.* I am saying how things have evolved. I am not saying how we humans morally ought to behave. I stress this, because I am in danger of being misunderstood by those people, all too numerous, who cannot distinguish a statement of belief in what is the case from an advocacy of what ought to be the case. My own feeling is that a human society based simply on the gene’s law of universal ruthless selfishness would be a very nasty society in which to live. But unfortunately, however much we may deplore something, it does not stop it being true. This book is mainly intended to be interesting, but if you would extract a moral from it, read it as a warning. Be warned that if you wish, as I do, to build a society in which individuals cooperate generously and unselfishly towards a common good, you can expect little help from biological nature. Let us try to teach generosity and altruism, because we are born selfish. Let us understand what our own selfish genes are up to, because we may then at least have the chance to upset their designs, something that no other species has ever aspired to.

As a corollary to these remarks about teaching, it is a fallacy— incidentally a very common one — to suppose that genetically inherited traits are by definition fixed and unmodifiable. Our genes may instruct us to be selfish, but we are not necessarily compelled to obey them all our lives. It may just be more difficult to learn altruism than it would be if we were genetically programmed to be altruistic. Among animals, man is uniquely dominated by culture, by influences learned and handed down. Some would say that culture is so important that genes, whether selfish or not, are virtually irrelevant to the understanding of human nature. Others would disagree. It all depends where you stand in the debate over ‘nature versus nurture’ as determinants of human attributes. This brings me to the second thing this book is not: it is not an advocacy of one position or another in the nature/nurture controversy. Naturally I have an opinion on this, but I am not going to express it, except insofar as it is implicit in the view of culture that I shall present in the final chapter. If genes really turn out to be totally irrelevant to the determination of modern human behaviour, if we really are unique among animals in this respect, it is, at the very least, still interesting to inquire about the rule to which we have so recently become the exception. And if our species is not so exceptional as we might like to think, it is even more important that we should study the rule.

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The third thing this book is not is a descriptive account of the detailed behaviour of man or of any other particular animal species. I shall use factual details only as illustrative examples. I shall not be saying: ‘If you look at the behaviour of baboons you will find it to be selfish; therefore the chances are that human behaviour is selfish also’. The logic of my ‘Chicago gangster’ argument is quite different. It is this. Humans and baboons have evolved by natural selection. If you look at the way natural selection works, it seems to follow that anything that has evolved by natural selection should be selfish. Therefore we must expect that when we go and look at the behaviour of baboons, humans, and all other living creatures, we shall find it to be selfish. If we find that our expectation is wrong, if we observe that human behaviour is truly altruistic, then we shall be faced with something puzzling, something that needs explaining.

© Richard Dawkins

Extract from ) in June 2026, available in hardback, paperback, and ebook formats, ÂŁ25.00

The Âé¶čŽ«Ăœ Book Club is reading The Selfish Gene in June. Sign up for the Book Club here, and join the discussion on Discord .

In 1976, published a book titled after an idea he’d come up with while teaching a lecture on animal behaviour for his PhD supervisor. It just so happened that the idea of The Selfish Gene was an irresistible scientific metaphor, and the book became a global bestseller. It remains one of the most thrilling popular books on evolution ever written.

After fifty years The Selfish Gene feels its age, but the core message remains relevant not just because genes being selfish is a brilliant meme (a term Dawkins coins at the end of the book), but because it is such a powerful way to understand how evolution operates: the metaphor makes us think as if genes behave selfishly. It makes us think from a gene’s-eye view. In doing so, Dawkins modernised evolutionary biology and also democratised it – he made it a thing of the people. Now anyone could grasp why vampire bats share blood with each other, why orchids mimic bees and why a cold virus makes us cough: why living things looked and behaved the way they did.

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When Charles Darwin set out his theory of natural selection, he did so by understanding that individuals compete for resources and that they differ in how they survive and in how many offspring they add to the next generation. Individual members of a species should behave for the good of themselves, said Darwin, not for the benefit of others, and traits that help individuals do better are passed on. Fine on the surface, but that didn’t always work– for example in insect societies where sterile workers labour to help a queen reproduce or even kill themselves to protect their nest. Darwin’s solution was to argue that in social insects, such as ants, wasps and bees, the family was effectively the individual, so sterile workers apparently helping the family were essentially helping themselves. It was a fudge, but he was on the right lines.

Over the middle part of the 20th century, as part of the revamping of evolutionary biology and its marriage with genetics that became known as the modern synthesis, a number of biologists mathematically described how evolution operates by changes in the frequency of genetic variants. Then two biologists in particular, George Williams and WD Hamilton, showed how understanding adaptations (structures, traits and behaviours that help organisms survive) as working for the benefit of the gene could explain apparent altruism. From the point of view of the gene, it makes sense for a worker ant to forgo reproduction and help her mother raise offspring, as she is helping her own genes into the next generation.

Darwin, without knowing about DNA or genes, had guessed what was happening. Dawkins brought the mathematics and theory beautifully to life. Out were the Lamarckian “just-so” stories about evolution (for example, that elephants got their long trunks from generations of stretching them), and out was the idea that organisms behaved for the good of the species; in was a graspable description of biology that aligned with the genetics.

One of the criticisms levelled at Dawkins, in building on the work of Williams and Hamilton, is that he merely popularised what others had devised. But The Selfish Gene acted as midwife to academic theory; it birthed a concept that influenced generations of biologists, and, importantly, the public.

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Another criticism is that the book’s idea of what a gene is, and how DNA works, is wrong or over-simplified. DNA does not work alone; a cell’s components act in symphony to produce a phenotype. The key quality of a gene is not its executive power, but its stability over time, the persistence of its genetic sequence. Dawkins knew this, but decided not to call the book The Immortal Gene.

Perhaps the biggest problem people now have with the book is that it popularised genetic animism– the belief that DNA commands the cell and the organism. In Dawkins’s telling we are “gigantic lumbering robots”, survival machines “blindly programmed to preserve the selfish molecules known as genes”. At best this is literary oversimplification. At worst, it supports an erroneous view of genetic determinism, the idea that aspects of our behaviour are inescapably programmed by our genes. We would see this again in the over-reach of the Human Genome Project, and the idea that there are genes “for” everything from heart disease to intelligence. That’s not how genes work.

Reading it today, I am struck too how the metaphor of selfishness underplays the role of cooperation and symbiosis in life. Dawkins addresses this in the text, but the power of his metaphor is such that this aspect is inevitably neglected.

These criticisms aside,Ìęthe way Dawkins so brilliantly and evocatively described animal behaviour from the perspective of the gene is why it hadÌęsuchÌęa huge influence. People forget that Dawkins was not a geneticist but an ethologist, he studied the evolutionary basis of animal behaviour.ÌęAs an undergraduate, it’s what got me hooked and made me become a behavioural ecologist. And that, for me, absolves most of the other stuff.ÌęIt is why, despite its datedness in parts, the metaphor still works.

Rowan Hooper’s book , is published in June.

We now have some of the most detailed maps ever made of several cancers, along with new tools and methods for analysing them. The findings come from an initiative to map cancers called the , and provide clues about how cancers form, evolve and become resistant to treatment.

Cancer develops when genetic mutations spur cells to grow and proliferate uncontrollably. Much of what we know about the disease comes from genetically analysing tumours. Until recently, we could only do this by combining and analysing all the genetic data in a tumour sample at once, making it impossible to identify individual cell types.

But tumours aren’t monolithic. “They’re complex, like ecosystems that consist of not just tumour cells, but also immune cells, endothelial cells and other support cells,” says at the Dana-Farber Cancer Institute in Boston.

Thanks to the advent of more sophisticated tools, a team of researchers has now been able to identify individual cells or determine their functions in tumours from nearly 2000 people with 20 different kinds of cancer.

As part of the work, at Washington University in St. Louis, Missouri, and her colleagues from 78 people with cancer types that show up in the breasts, colon, pancreas, kidneys, uterus and the bile ducts that connect the liver and gall bladder to the small intestine. They used a technique called single-cell sequencing to measure which genes were turned on or off in each cell of a tumour sample.

The researchers also viewed tissue samples under powerful microscopes to determine the location and structure of cells. Next, they built 3D models of tumours, showing how cells within them are organised and interact. They found that, within tumours, cancer cells form distinct clusters known as microregions. The researchers then grouped these areas based on similar genetic alterations, such as high or low immune cell activity. Evolution within the genetic activity of cells in microregions appears to be a major factor in cancers becoming resistant to treatments.

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Further research from the Human Tumor Atlas Network suggests that to form colon cancer. “For decades, the consensus in the field has been that a tumour originates from a single cell,” says at the University of Cambridge.

Winton and his colleagues used mice that were genetically engineered so their cells changed colour when they became cancerous. This made it possible to identify and track tumours as they formed in the guts of the animals. The researchers found that about 40 per cent of colon tumours originated from multiple cells, which cooperated to outcompete neighbouring cells.

A separate group of researchers led by at Vanderbilt University in Tennessee also for monitoring tumour evolution. Naturally occurring mutations create permanent genetic changes in tissue, which allowed the researchers to reconstruct the sequence of events, creating a molecular timeline of each tumour’s growth.

Using this approach, they analysed early precursors of colon cancer in mice and people and found that up to 30 per cent had a multicellular origin. The best predictor we currently have for determining whether a precancerous lesion in the colon will become cancerous is its size, says Lau. Understanding how colon cancer forms can improve our ability to screen precancerous lesions and detect cancer earlier, he says.

The cancer mapping project uncovered some surprises. Abravanel and his colleagues collected 67 tumour biopsies from 60 people with , meaning it had spread to other organs, such as the liver, brain and lungs. They found that samples collected from the same participant at different time points were genetically very similar. “You would expect to see different mutations evolve over time,” says Abravanel.

As part of the project, researchers led by at Princeton University that quantifies the proportion of cancerous and non-cancerous cells in a tumour and investigates how these cells interact, which can also help discern how a tumour is growing.

Together, these discoveries bring us a step closer to understanding how cancer forms and evolves, which, in turn, could improve treatment. Abravanel says this could help in his clinical practice as well: “We try as best we can to match the right treatment to the right patient, but largely we aren’t able to, for individual cases, pull out what the best therapy would be at that moment in time.”

Five genetic variants may be linked to the onset of short-sightedness in people who study to university level. The discovery could help to identify children who are more likely to develop the condition so that interventions can be put in place to help prevent its onset, such as spending more time outdoors.

Short-sightedness, also called myopia, is a common condition that affects a person’s ability to see distant objects.

Prior to this research, genetics and lifestyle factors were thought to affect our myopia risk. at Cardiff University, UK, and her colleagues wanted to better understand how these factors interact to influence the condition’s onset.

The team conducted a genome-wide association study (GWAS) on people with European ancestry. These scan markers across genomes to find any variations associated with a particular condition.

The researchers first looked for genetic variants linked to myopia in more than 88,000 adults, assessing whether the participants had myopia according to a standard eye test.

They identified 19 variants that are linked to different severities of myopia when they interact with certain environmental factors or other genes.

Finally, the team analysed these variants in more than 250,000 people who wore glasses. “We generally took people who said they started wearing glasses before 25 as a sign they had myopia,” says Clark.

The researchers were particularly interested in a potential three-way link between genetic variants, education level and myopia.

The participants therefore also reported whether they went to university. “Many studies have shown the link between education and myopia,” says Clark. More time in education is usually linked to more time indoors, she says. We know that frequently spending time outdoors may prevent myopia’s onset or stop it worsening.

The results suggest five of the 19 genetic variants are affected by education level and together these are linked to myopia.

Two of the variants were identified in a looking at myopia in people of east Asian ancestry.

Some of these five variants are linked to the visual system, but it is unclear how they may cause myopia, says Clark.

The findings may not apply to people of non-European descent, she says. About 30 per cent of children in the West develop myopia compared with 80 per cent of children in east Asia, says Clark.

Nevertheless, identifying these genetic variants could one day help researchers determine a child’s myopia risk.

“Maybe the child could learn outdoors or we’re going to make sure the child takes regular breaks and has time [during the school day] to go outside,” says Clark.

at the Australian National University in Canberra is unsure whether this research has practical applications. “While this is beautiful scientific work that certainly adds to our understanding, the bottom line is that it is not clear that genetic analysis is leading to useful interventions to control myopia,” he says.

Researchers have developed a method that can turn back the biological clock on skin cells by 30 years, creating stem cells from mature ones, which could be used to treat skin conditions in the future.

In 2007, Shinya Yamanaka at Kyoto University in Japan developed a technique that could transform adult skins cells into stem cells by inserting four specialist molecules, dubbed “Yamanaka factors”, that reverse cell development. It takes around 50 days of exposure to these molecules for normal cells to be reprogrammed into what are known as induced pluripotent stem cells (iPSCs).

“When you turn to a cell into an iPSC, you lose the original cell type and its functionality,” says at the Babraham Institute in Cambridge, UK.

Gill and his colleagues have now devised a technique that uses Yamanaka factors to rejuvenate skin cells without losing their previous functionality.

The researchers collected skin cell samples from three human donors that had an average age of around 50, then exposed these to the Yamanaka factors for just 13 days to partially anti-age the cells. They then removed the Yamanaka factors and left the cells to grow.

As we age, our DNA gets tagged with chemicals, so tracking these markers can help us determine how old our bodies are. This is known as our epigenetic clock. Over time, some of our genes will either turn on or off, the collection of which is known as the transcriptome.

Gill and his team found that the epigenetic clock and transcriptome profiles of the partially reprogrammed cells matched the profiles of skin cells that belonged to people who were 30 years younger.

The rejuvenated cells also functioned like younger ones, too, creating more collagen than those that didn’t undergo reprogramming. And when placed onto an artificial wound, the reprogrammed cells moved to close the gap much quicker than the older ones did.

“In young people, if you cut yourself, it’ll take quicker to heal the wound, while it would take me longer to heal,” says team member , also at the Babraham Institute. “It’s very exciting – not only the molecular read-outs that are younger, but the cell also functions more like young cells.”

The key advance in this study is that we are now able to substantially rejuvenate cells without changing their identity or functionality, says Reik. “In previous studies, you would end up with a stem cell, which is not what you’d want for therapy.”

The technique may one day be useful in treating skin conditions, such as burns and ulcers. There is also the added bonus that the cells wouldnt be rejected by an individual’s body, because they would be their own cells, says Gill.

“So far, we’ve only tested this technique in skin cells. We’re excited to see if we can translate it across other cell types,” says Gill.