Research indicates that Vγ4+ γδ T cells in NOD mice can suppress T1DM development by producing IL-17 and facilitating the differentiation of regulatory CD4+ αβ T cells in pancreatic lymph nodes; Vγ1+ cells, biased toward IFN-γ production, thereby promote a pro-inflammatory microenvironment conducive to T1DM pathogenesis (51). Here, IFNG is linked to type 1 diabetes mellitus.