Sorafenib was originally developed as an anti-cancer drug aiming at growth suppression by inhibiting a multitude of different kinases, among which are VEGFR, PDGFR and Raf family kinases.[37] As shown in Fig 7B, 1μM Sorafenib significantly downregulated mRNA expression of Il-1 and 6, Cxcl1, S100a9 and Hif1α, but did not prevent the downregulation of Acta2, Cnn1 or Nr4a1 mRNA, and therefore did not prevent the VSMC phenotype switch. The gene discussed is ACTA2; the disease is cancer.