In the current study, we generated a Palm-stress paradigm in L6-GLUT4myc myotubes and myoblasts that recapitulates the loss of DOC2B protein abundance observed in human T2D skeletal muscle [14], as well as the affiliated dysregulated GLUT4 vesicle exocytosis and glucose uptake. This evidence concerns the gene DOC2B and type 2 diabetes mellitus.