Although multiple studies reported that PPARγ competitively inhibited the inflammatory signal pathway including NF-κB, JAK-STAT, NFTA (nuclear factor of activated T cell), and AP-1 (Activator protein-1), thereby alleviating inflammatory response and pathological damage of atherosclerosis [37–40], others suggested the activation of PPARγ exerted pro-inflammatory and pro-atherosclerotic effects [36]. Here, SOAT1 is linked to atherosclerosis.