Furthermore, a 1-3% population of insulin-binding B cells forms in the periphery of non-autoimmune, T1D-protected VH125SD.C57BL/6 mice, which lack the critical IAg7 MHC class II molecule necessary for proinflammatory islet-reactive T cell activation and spontaneous diabetes development 43, further highlighting the T cell independence of insulin-binding B cell formation in this BCR transgenic model. The gene discussed is INS; the disease is type 1 diabetes mellitus.