A prevailing sentiment in the endophenotype literature is that psychiatric endophenotypes are somehow different from clinical phenotypes and other complex traits. Endophenotypes are promoted precisely because they are expected to be more proximal to gene action and thus more heavily influenced by particular genetic variants. That is, genetic effects are expected to be larger, much larger even, than the effects of more distal phenotypes. Although this may well prove to be true, the empirical literature available to date suggests otherwise.
