Unlike our observations that mFicDR371S mice islet organization involves population changes in both α-cells and δ-cells and becomes more disordered with age, NOD Ire1αβ−/− islets appear to exhibit only a transient defects in insulin secretion and islet disorganization, which recovers over time and is protective from insulitis and the development of type I diabetes [12]. This evidence concerns the gene INS and type 1 diabetes mellitus.