ABCA1 and atherosclerosis: In the mouse model of atherosclerosis, the expression of sEH is elevated in foam cells, and the elevated activity of sEH-P dephosphorylates ABCA1, increases the stability of ABCA1, and enhances cholesterol efflux, thereby attenuating cholesterol accumulation in the macrophage, decreasing foam cell formation, and slowing down the progression of atherosclerosis, at which time the activity of sEH-P plays a protective role in atherosclerosis (Lien et al., 2019).