UCMD fibroblasts isolated from the skin, and differentially from tendons, do not exhibit defects in the collagen VI-NG2 (neural/glial antigen 2) axis that affects cell polarization during migration in response to in vitro injuries [7] and do not show the mitochondria defects [8] observed in skeletal muscle fibers and myoblast cultures of Col6a1−/− mice and in muscle cell cultures from patients affected by ColVI myopathies [9]. The gene discussed is COL6A1; the disease is Congenital muscular dystrophy, Ullrich type.