HGF is highly expressed in the liver microenvironment and can facilitate tumor growth.[43] Moreover, the HGF/c‐Met pathway is one of the most important RTK pathways in both the liver and advanced hepatocellular carcinoma.[44] Recombinant HGF did not affect PU.1 expression (Figure 6B) but significantly enhanced PU.1 phosphorylation in HT29 and CRC57 cells, which was abrogated by the c‐Met inhibitor PHA665752 (Figure 6C). The gene discussed is SPI1; the disease is neoplasm.