In addition, CD4+LAP+ (latency-associated peptide) Tregs have been identified recently as the third iTregs subtype whose suppression is mediated by TGF-β in immune diseases including experimental autoimmune encephalitis (EAE), type I diabetes mellitus (T1DM), systemic lupus erythematosus (SLE), collagen-induced arthritis, type II diabetes, and atherosclerosis in mice [74,89]. This evidence concerns the gene TGFB1 and type 1 diabetes mellitus.