Elevated SAC currents have been detected in δ-SG-deficient myotubes [85], and although transient receptor potential canonical 1 (TRPC1) has been suggested as a candidate SAC involved in the pathogenesis of the mdx mouse model of DMD and cardiomyopathy [86,87], there have been no studies of this channel in δ-sarcoglycanopathy. Here, ADCY10 is linked to Duchenne muscular dystrophy.