However, during early steps of myogenesis, myoblasts largely express T-type calcium channels instead of Cav1.1 and provide hyperpolarization to fusion-competent myoblasts.11 In addition, the resting membrane potential is unchanged between normal and DM1 myoblasts.12 Although these electrophysiological observations in DM1 hint towards a role in myopathy, they are not sufficient to explain muscle wasting. The gene discussed is CACNA1S; the disease is myotonic dystrophy type 1.