We hypothesized that as PPARα appears to be required for the full deleterious effect of the RAS, the double ApoE/PPARα knockout (DKO) mouse should be resistant to the worsening of atherosclerosis induced by chronic inhibition of endothelial NOS (eNOS) activity by a subpressor dose of Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME). Here, APOE is linked to atherosclerosis.