The IL-12–IL-18–T-bet–IFN-γ pathway is a powerful proinflammatory stimulus that promotes and accelerates lesion development, and atherosclerosis is reduced by disruption of the IL12 gene in ApoE−/− mice [350] or by functional blockade of IL-12 with anti-IL-12 antibodies [351], accompanied by increased plaque stability, as indicated by augmented collagen levels. This evidence concerns the gene IL18 and atherosclerosis.