In murine models of T1DM, EVs that originated from bone marrow-derived MSCs resulted in a delayed onset of T1DM, the preservation of islet cells, the reduction in insulitis and T cell infiltration, the decrease in antigen-presenting cell (APC) and T cell activation, lessening the Th1/Th17 population, and a decline in the production of inflammatory cytokines including IL-17, IL-6, IFNγ, TNFα, and IL-12 [124]. This evidence concerns the gene IL17A and type 1 diabetes mellitus.