If this rapid GC effect on dysferlin-deficient adipocytes occurs in human muscles (as observed after 3 months in dysferlin-deficient mice [37]), then many months of clinical administration of GCs might exacerbate the replacement of dysferlin-deficient myofibres by dysferlin-deficient adipocytes, and contribute to the reported histopathology and loss of muscle function in humans with dysferlinopathy [33]. This evidence concerns the gene DYSF and neuromuscular disease caused by qualitative or quantitative defects of dysferlin.