Our ΔHel1 mouse validated and expanded upon previous findings by Lincez et al. with NOD.MDA5+/– mice, which had delayed spontaneous and CVB4-accelerated T1D due to decreased MDA5 expression, had reduced Ifna mRNA, had a dampened CD4+ T cell effector response, and had a concomitant increase in Treg populations in the PLNs (13). Here, IFNA1 is linked to type 1 diabetes mellitus.