They demonstrated that stimulation of normal fibroblasts with these molecules resulted in downregulation of miR-29a similar to levels seen in SSc fibroblasts, whereas inhibition of TGF-β and PDGF-B pathways with imatinib restored miR-29a levels in SSc fibroblasts as well as bleomycin-induced skin fibrosis. Here, TGFB1 is linked to systemic sclerosis.