Moreover, it was demonstrated that SSc BM-MSCs express higher levels of ADAM12 in respect to healthy MSCs and that a pathologic microenvironment enriched in TGF-β1 may contribute to pericyte-to-myofibroblast differentiation by further increasing ADAM12 expression, which indeed acts as a positive regulator of the profibrotic TGF-β1 signaling cascade [97]. The gene discussed is TGFB1; the disease is systemic sclerosis.