Moreover, the above mechanism of inhibition of non-canonical and canonical TGF-β1 signaling by sildenafil, SB204741, and their combination might be a possible explanation for the amelioration of ACTA2 gene expression, leading to a decrease in ECM production as well as a decrease in the production of proinflammatory cytokines in our experimental model of PF (Figure 10). The gene discussed is ACTA2; the disease is pemphigus foliaceus.