The lower suppressive capacity of Tregs from T1D patients, their phenotypic shift accompanied by decreased production of anti-inflammatory cytokines IL-10, IL-35 and TGF-β and increased production of inflammatory cytokines IFN-γ and IL-17 (84, 86–89), unstable FoxP3 expression (90), and higher susceptibility to apoptosis were documented (91–95). This evidence concerns the gene FOXP3 and type 1 diabetes mellitus.