Many of these differences implicated at the pathway level, particularly the increased conversion of cholesterol to primary bile acids, decreased sterol and unsaturated fatty acid synthesis, decreased PPAR signaling (also seen in analysis of individual PPARα and γ targets in Table 1), and decreased inflammation in the NCoRδ-/- versus the NCoRω-/- mice, are highly consistent with, and likely contributory to, their distinct hepatic steatosis phenotypes. This evidence concerns the gene PPARA and Hepatic steatosis.