the potential role of the gene in AD because it fails to take into account how broader gene networks function. Because genes act together in biological networks to perform a particular function, we reasoned that if a biological process is important in modulating the propensity to develop AD, then variation in any genes similarly affecting that process might cause a similar change in the liability to develop AD. We therefore tested all members of the SWI/SNF chromatin remodeling complex as a set to evaluate association with AD and a related phenotype in two human samples because we had evidence from our model organism work that this complex is involved in the behavioral response to ethanol, and we had previously observed an association with two members of the SWI/SNF complex and AD in the IASPSAD study (Mathies et al., 2015).