Given that skeletal t-tubules express endogenous BIN1 (23, 35) and that insulin-stimulated GLUT4 translocation increases glucose utilization in skeletal muscle (36), it will be compelling to explore whether skeletal muscle transduction of cBIN1 or the equivalent skeletal isoform of BIN1 provides additional benefit in hyperglycemic control in T2DM. This evidence concerns the gene BIN1 and type 2 diabetes mellitus.