Concerning the mechanisms proposed to link CHIP and cardiovascular events, it has been observed that in mice engineered to bear mutations in genes commonly involved in CHIP (e.g., Tet2), there was an increased expression of proinflammatory mediators implicated in the pathogenesis of atherosclerosis, such as cytokines interleukin (IL)-1b and IL-6 [117]. This evidence concerns the gene STUB1 and atherosclerosis.