[23, 24] The VEGF-mediated pathway was observed to be enhanced in the tumor angiogenesis of HCC.[25, 26] Additionally, high VEGF plasma levels are correlated with poor survival of patients with HCC.[27] A multikinase inhibitor that suppresses the phosphorylation of VEGF receptor 2 and EGF receptor was suggested to be a potential chemotherapeutic agent for HCC.[28] Taken together, the EGF- and VEGF-pathways may be critically involved in the inflammation-induced procarcinogenic process in chronic hepatitis B. The gene discussed is EGF; the disease is chronic hepatitis B virus infection.