T1D results from the loss of pancreatic islet β-cells, often through autoimmune activation, β-cell autoantigen release, oxidative and endoplasmic reticulum (ER) stress, and cytokine-mediated damage, leading to β-cell destruction, insulin deficiency, and hyperglycemia through disruption of insulin signaling pathways (Figure 1) [5,6,7,8]. Here, INS is linked to Hyperglycemia.