In vitro studies showed that pirfenidone inhibited PSC proliferation, invasion, and migration, and interrupted the interaction between pancreatic cancer cells and PSCs; these effects were associated with decreased expression of PDGF-A, HGF, periostin, collagen type I, and fibronectin in PSCs, as well as reduced PSC activation (decreased α-SMA expression) (Kozono et al., 2013). The gene discussed is ACTA1; the disease is familial pancreatic carcinoma.