For example, IL-17A−/−Ldlr−/− mice demonstrated a similar plaque burden within the aortic roots or descending aorta with that of Ldlr−/− mice although their aortic macrophages, CD11b+DCs, and T cells were reduced (113), whereas IL-17A−/− ApoE−/− or IL-17RA−/−ApoE−/− mice manifested reduced atherosclerosis by 35 or 25%, respectively, indicating a pro-atherosclerotic role of IL-17A signaling (114). The gene discussed is LDLR; the disease is atherosclerosis.