Although the absence of proprotein convertase subtilisin/kexin type 9 in atherosclerosis-prone Ldlr−/−Apobec1−/− mice esulted in decreased lipid and apoB levels, fewer atherogenic LDLs, and reduced atherosclerosis, the LDLs from these mice could induce lower endothelial expression of intercellular adhesion molecule-1, CCL2, CCL7, IL-6, and IL-1β [45]. The gene discussed is CCL2; the disease is atherosclerosis.