In contrast to cardiovascular effects seen in Tet2-deficient mouse models, neither an unusual predisposition to atherosclerosis nor an abnormal pro-inflammatory cytokine or chemokine expression was observed in seven individuals of a family with genetic predisposition for lymphoma development and germline haploinsufficiency of TET2. Despite the small number of individuals studied, these data raise the possibility that additionally accumulated changes in CHIP clones might be relevant to the atherogenic effect observed in humans [42]. The gene discussed is TET2; the disease is atherosclerosis.