Indeed, while few cells co-expressing the TC marker CD34 and the myofibroblast marker α-smooth muscle actin (α-SMA) have been detected in fibrotic SSc skin and in bleomycin-treated mouse skin at early stages of the fibrogenic process [13,20], in dermal lesions of both SSc patients and bleomycin-induced mouse model TEM analysis provided clear evidence of progressive degenerative ultrastructural changes and necrosis of TCs rather than their transdifferentiation into profibrotic myofibroblasts [19,20]. This evidence concerns the gene ACTA1 and systemic sclerosis.