Of the 33 putative interacting proteins identified following immunoprecipitation of β2*-nAChRs from human cortex (Table 3), 14 proteins differed in interaction as a result of tobacco use, as measured by a shift in the ratio of the interacting protein to nAChR number between nonexposed and tobacco-exposed individuals, with two additional protein (14-3-3ζ and ATP1A2) that showed a significant nicotine × mood disorder interaction (Fig. 4A, Table 7). The gene discussed is ATP1A2; the disease is mood disorder.