explicitly the chief programmatic fallacy committed by those who argue so strongly for the importance of heritability measures for human traits. The fallacy is that a knowledge of the heritability of some trait in a population provides an index of the efficacy of environmental or clinical intervention in altering the trait either in individuals or in the population as a whole. This fallacy, sometimes propagated even by geneticists, who should know better, arises from the confusion between the technical meaning of heritablility and the everyday meaning of the word. A trait can have a heritability of 1.0 in a population at some time, yet this could be completely altered in the future by a simple environmental change. If this were not the case, ‘inborn errors of metabolism’ would be forever incurable, which is patently untrue. But the misunderstanding about the relationship between heritability and phenotypic plasticity is not simply the result of an ignorance of genetics on the part of psychologists and electronic engineers. It arises from the entire system of analysis of causes through linear models, embodied in the analysis of variance and covariance and in path analysis. It is indeed ironic that while Morton and his colleagues dispute the erroneous programmatic conclusions that are drawn from the analysis of human phenotypic variation, they nevertheless rely heavily for their analytic techniques on the very linear models that are responsible for the confusion. I would like to look rather closely at the problem of the analysis of causes in human genetics and to try to understand how the underlying model of this analysis moulds our view of the real world. I will begin by saying some very obvious and elementary things about causes, but I will come thereby to some very annoying conclusions.