Baseline expression differences between LCLs derived from AD subjects vs. controls could result either from pre-existing genetic differences that affect risk for AD or from effects of the long-term alcohol exposure of the AD subjects from whom they came. Transformation and growth of the LCL would be expected to reduce differences due to the previous drinking history. Differences were, in fact, small and our data both here and in the previous experiment on LCLs from the same individuals (McClintick et al., 2014) were underpowered to identify them. Even combining the data on unexposed cells identified only 9 genes with an FDR < 0.20 (Table 3, Supplemental table S4). To see if there were suggestions of effects, we relaxed the criteria for this combined analysis to p< 0.05; 465 genes showed differences ≥1.2-fold. TMOD2, CLIC2, NPNT, EIF1AY, FYB, TANC1 and KCNA1 were expressed at much lower levels in cells from AD, and WFDC2, TIE1, ASB2, MUC13, and FOXA3 were expressed at much higher levels (Table 3).
