It is tempting to speculate that Ide may be required to control mRNA processing and, through it, metabolism and insulin production in Ins+ beta cells, explaining that its loss results in beta-cell hypertrophy, unbridled mTOR activation, and (pro-)insulin production and diabetes in Ide−/− C57BL/6 mice fed a high-fat diet [4]. This evidence concerns the gene INS and diabetes mellitus.