Numerous studies also confirm ApoE4 plays a role in NF-κB–mediated transcription of genes associated with increased inflammatory cytokine release (59, 60), thus suggesting both endogenous ApoE and ApoE polymorphisms produce significant differences and a possible mechanistic pathway through which ApoE4 may influence DCM pathophysiology. The gene discussed is NFKB1; the disease is familial dilated cardiomyopathy.