The observation that in the ApoE−/− (apolipoprotein E-deficient) mouse model, which is a model prone to accelerated atherosclerosis, IL-17A blockage reduced the plaque burden, IL-6 levels, G-CSF levels, CXCL1 expression, and macrophage content in the aorta strongly suggests, among many others, a pathogenetic role of IL-17A in the atherogenic process (74). The gene discussed is IL17A; the disease is atherosclerosis.