She picked up her proofs again. Her book on epigenetics suddenly seemed like a refuge rather than a chore. Since the millennial utopianism that had greeted the completion of the Human Genome Project twenty years ago, the search for the genes that corresponded to every desire and disease, every inclination and physical feature, had been, with a few exceptions, a failure. When Svante Pääbo had been in charge of the chimpanzee genome project, he had expected to find ‘the profoundly interesting genetic prerequisites that make us different from other animals’, but ended up, after the chimpanzee sequence was published, admitting that ‘we cannot see in this why we are so different from chimpanzees’. Not only did we turn out to share almost all of our genes with our fellow primates, but with far more distant relatives as well. The homeobox genes, which determine the position of limbs and other body segments, were almost identical in flies, reptiles, mice and humans. Where most variation was expected, there was least change. Nor was the quantity of human intelligence and self-regard reflected in the quantity of its genes. When the human genome had been sequenced, it turned out to contain twenty-three thousand genes, about the same as a sea urchin’s, but drastically fewer than the forty thousand in rice.

Ah, yes, here it was, the key paper in Nature on missing heritability (Manolio, et al.), that ended with the sublime sentence, ‘Given how little has actually been explained of the demonstrable genetic influences on most common diseases, despite identification of hundreds of associated genetic variants, the search for the missing heritability provides a potentially valuable path towards further discoveries.’ In what other field of science would something be demonstrable ‘given how little has actually been explained’? In what other scientific field would lack of evidence be described as ‘a potentially valuable path’, except in the sense that all paths that had no actual value could only be ‘potentially’ valuable? It was amazing that a journal which stood for the highest standards of scientific rigour would publish such an incompetently devious sentence. A more honest version would have been, ‘After decades of research, we’ve found almost nothing, but we’ve devoted our careers to this fruitless field, so please give us more money.’ Of course, some evidence might turn up in the future but one of the most valuable contributions made by genetic studies was to show that so far there was no purely genetic influence on the formation of all but rare monogenic diseases, like Tay-Sachs, haemophilia and Huntington’s, known to be caused by a mutation in a single gene; and there was the extra copy of chromosome twenty-one that produced Down’s syndrome, but after these simple certainties, ‘polygenic scores’ and ‘multifactorial’ explanations had to be brought in to prop up the plausibility of the genetically determined story.