  At the level of the organism, talk of genetic coding and the asymmetry between genetic and nongenetic causes such talk conveys, even when countenanced at the cellular level, are deemed less acceptable (Godfrey-Smith 2000). New research in functional genomics may well lead to less deterministic accounts even of so-called single gene disorders. For these, the concepts of penetrance and expressivity operate in ways which accommodate the one-one genetic determinist model where the mutation is necessary and/or sufficient for both the presence of the condition and confounding patterns of phenotypic variability. But the severity of even a fully penetrant condition like Huntington's disease seems to depend on not just genetic factors like the number of DNA repeats in the mutation but epigenetic factors like the sex of the parent who transmitted the mutation (Ridley et al. 1991).