It has long been established that administration of low‐dose IL‐2 is beneficial for tolerance induction in T1D,[36] and inhibition of T‐cell TGF‐β1 signaling would lead to development of autoimmune phenotype.[25b] As a result, considering that both TGF‐β1 and IL‐2 are essential for the development and function of Treg and immune tolerance, our observation supports a facilitative role of Nap‐GdFdFdY in Treg function during hyperglycemia. Here, TGFB1 is linked to type 1 diabetes mellitus.