UFP further modulated lipid metabolism and the antioxidant property of HDL, while administration of D-4F, an apolipoprotein A-I (ApoA-I) mimetic peptide, attenuated UFP-modulated lipid metabolism and atherosclerosis (Li et al. 2013), which is consistent with studies demonstrating that D-4F restored HDL function and attenuated atherosclerosis (Morgantini et al. 2011; Navab et al. 2002). Here, APOA1 is linked to atherosclerosis.