The critical role of this protein is underscored by findings that muscular insulin sensitivity is strongly correlated to GLUT4 protein content (Kraegen et al., 1993), impaired insulin stimulated GLUT4 PM trafficking in the skeletal muscle of T2D is the primary defect defining this disease (Garvey et al., 1998; Gould, Brodsky & Bryant, 2020) and that GLUT4 protein overexpression preserves systemic insulin sensitivity in a commonly employed mouse model of diabetes (Atkinson et al., 2013). Here, INS is linked to diabetes mellitus.