As discussed in the context of adult models, the increased risk of insulin-resistant diabetes in the elder model is supported by the following three points: (1) multi-omics data, which includes multiple altered proteins and metabolites implicated in insulin-resistant (Fig. 7d, e, Supplementary Figs. 4 and 5); (2) pathological phenotypes reminiscent of Type 2 diabetes, such as inflammation and amyloid deposition; and (3) corroborating results from other research groups.42,52 Amyloid deposition within islets in Type 2 diabetes typically commences in and around the capillaries and between cells. The gene discussed is INS; the disease is insulin-resistant diabetes mellitus.