Similar to Pparα- andPgc1α-deficient mice (Akiyama et al., 2001; Costet et al.,1998; Kim et al., 2003; Lee et al., 1995; Leone et al., 2005), fat accumulation is more pronounced inRap1-deficient females than in males, and they developpathologies that are reminiscent of metabolic syndrome in humans, further supportingthat RAP1 and PPARα are in the same pathway for regulation ofmetabolism. The gene discussed is PPARA; the disease is metabolic syndrome.