On the other hand, the lack of a proper remodeling of actin in UCMD TFs might have negative consequences on the subcellular redistribution of proteins, such as Akt [55], as well as of organelles, including mitochondria [56] and autophagosomes [57], whose activities are altered in Col6 null mice [1,11] and in patients affected by COL6-RMs [58]. Here, AKT1 is linked to Ullrich congenital muscular dystrophy.