Specific LysMCre-driven deletion of Tet2 in Tregs led to deranged suppressor function, phenotypic dysregulation and eventually to a phenotypic switch toward a proinflammatory TH17/TFH effector phenotype (148), similar to what has been described for pathogenic ApoB-reactive autoimmunity in atherosclerosis (96). Here, APOB is linked to atherosclerosis.