We and other have reported a number of potential intrinsic defects in myotubes established from patients with T2D including impaired insulin-stimulated glycogen synthesis [20]; reduced glycogen synthase activity [20]–[22]; reduced basal glucose uptake [20]; impaired glucose oxidation [23], a reduced TCA flux [24]–[25] and a lower basal palmitate oxidation [26], [27]–[28]. The gene discussed is INS; the disease is type 2 diabetes mellitus.