Research has shown that mutations in the c-Maf protein’s SUMO modification sites (KRc) in NOD mice accelerate diabetes onset by suppressing the recruitment of the repressive complex death-associated protein (DAP)/histone deacetylase 2 (HDAC2) and enhancing the activation of IL-21 as well as the recruitment of coactivators cAMP response element-binding protein-binding protein (CBP) and p300 to the IL-21 promoter’s MARE region (91). Here, IL21 is linked to diabetes mellitus.