Suppressing RAD51 with CRISPR/cas9 and inhibitors (such as 4,4’-diisothiocyanatostilbene-2, 2’-disulfonic acid) decreases the diabetes process by reducing diabetogenic T cell responses via expanding CD73+ B lymphocytes that exert regulatory activity in T1DM-susceptible nonobese diabetic (NOD) mice (14). Here, RAD51 is linked to diabetes mellitus.