Our data currently cannot distinguish between these and other possible models. However, the original observations that led to the current studies do suggest that the effects of variation in SWI/SNF complex members on AD may be, at least in part, through the modulation of the physiological response to the drug itself. We previously found that in the model organism C. elegans, the acute physiological response to alcohol is altered in animals with altered SWI/SNF function. Animals with loss of function of the BAF complex have decreased initial sensitivity to ethanol, while loss of function of the PBAF complex eliminates the ability of animals to develop AFT to ethanol (Mathies et al., 2015). Although the direct relationship between acute ethanol response phenotypes in C. elegans and human AD is not clear, empirically, a finding that a gene has an effect on acute alcohol response phenotypes in invertebrate model organisms very strongly predicts that variation in that gene will be implicated in human AD (Grotewiel and Bettinger, 2015). This empirically observed relationship between genes affecting acute alcohol responses in model organisms and
