Similar to dysferlin-deficient LGMD2B and DMD, we identified that sarcolemmal repair deficits are a feature of the FSHD patient myoblasts and of skeletal muscle from a mouse model of FSHD (FLExDUX4) that presents with evidence of a slow myopathy (e.g., a significant increase in skeletal muscle fibrosis) [19,20,35]. This evidence concerns the gene DYSF and Duchenne muscular dystrophy.