This finding is especially important in the context of autoimmunity, as Th1 and Th17 effectors have been associated with several autoimmune diseases, including T1D and MS, suggesting that CD4+CD25+CD226- Treg isolation may potentially deplete these pathogenic Tregs and present reduced risk of pro-inflammatory ex-Treg outgrowth compared to CD4+CD25+CD127lo/- Treg isolation (68–70). This evidence concerns the gene IL2RA and type 1 diabetes mellitus.