Further, our findings that MafB can promote macrophage cholesterol efflux in both LXR-dependent and independent manners, combined with the findings that MafB expression remains suppressed in oxidized cholesterol-laden or pro-inflammatory macrophages, may offer novel therapeutic opportunities to improve current treatment strategies for atherosclerosis via enhancing MafB-dependent signaling. The gene discussed is MAFB; the disease is atherosclerosis.