COL6A1 and Ullrich congenital muscular dystrophy: This kind of approach was fundamental for the design of pilot clinical trials based on the use of cyclosporin A [68] to reverse the mitochondrial dysfunction found in muscle cell cultures from Col6a1 null mice and UCMD patients [69], or on the application of a low-protein nutritional approach [70], to counteract the autophagic defects found in myofibers of Col6a1 null mice [70] and BM/UCMD patients [71].