The contemporary view of the involvement of the renin–angiotensin system in cancer, particularly HCC, might involve EGFR transactivation by AT1R and angiotensin II-independent, antiangiogenic effects of angiotensinogen [6, 41].The microenvironment in hepatocarcinogenesis becomes more complex in cases of viral infection and involves the transactivation of transcription factors and stimulation of inflammatory responses, thus resulting in oxidative damage, fibrosis, and genetic mutations [42]. This evidence concerns the gene AGT and hepatocellular carcinoma.