The possibility of a direct anti-atherosclerosis effect of the MK2 inhibitors, i.e., independent of lipid-lowering, is supported by a study in which genetic targeting of MK2 led to decreased lesion area in fat-fed Ldlr-/- mice, as, curiously, plasma lipids were actually higher, not lower, in the Mapkapk2-/-Ldlr-/- mice used in this study [14]. The gene discussed is MAPKAPK2; the disease is atherosclerosis.