For over 150 years, psychiatric researchers have noted familial patterns of inheritance in schizophrenia, once known as dementia praecox. In certain families in which the disease was common there appeared to be a decrease in age of onset of the illness from one generation to the next, a pattern known as ‘anticipation’. By the mid-twentieth century findings of anticipation had fallen into disrepute and were believed to be the result of statistical bias rather than biological reality. This changed in the early 1990s with the discovery of a unique form of dynamic mutation in two other diseases which had been associated with genetic anticipation – myotonic dystrophy and Huntington’s disease. Having found a causative mechanism which related the decreased age of onset of illness to the increasing size of DNA repeats within the disease gene from one generation to the next, researchers set out to discover if similar mutations lay behind findings of anticipation in other diseases, including schizophrenia. In spite of the best efforts of several groups of researchers, no such mutation has yet been found. This has led to a clash of opinions within the field between those who insist that their clinical findings of anticipation in families suffering from schizophrenia are accurate and those who deny those findings based on statistical arguments and the lack of an acceptable biological mechanism. I intend to use this case study to explore the ways in which knowledge is created in the field of medicine and to examine how current approaches tend to privilege the findings of molecular genetics and downplay the value of clinical observation.