Early mechanism dissection suggested that Sorafenib might function through inhibiting Raf‐1 and B‐Raf and the receptor tyrosine kinase activity of VEGFRs 1, 2 and 3 and PDGFR‐β.39, 40 However, recent reports indicated that STAT3 activation also played a key role in the development of Sorafenib resistance in HCC cell lines.19, 31, 32 Our clinical studies using human HCC samples also demonstrated that higher expression of activated p‐STAT3 might indicate worse recurrence free survival under Sorafenib treatment. The gene discussed is RAF1; the disease is hepatocellular carcinoma.