Genes that differ between alcoholics and controls were harder to detect, given the relatively high level of expression heterogeneity observed among all subjects. Such differences could reflect genomic variation between subjects including gene expression differences and gene product variations that contribute to risk, effects of repeated exposure to ethanol in the subject from whom the cells were derived, or gene x environment interactions. Most of the pathways that exhibited expression differences between LCLs from alcoholics and controls are signaling pathways, including ones associated with brain functions (Table 2). PRKCE is known to affect ethanol consumption (Olive et al., 2000).
