TERT and hepatocellular carcinoma: Mechanistically, androgen and its receptor could bind to two androgen-responsive element motifs within the genomic region of the HBV enhancer I to increase the HBV titer and enhance the transcription of TERT, whose activation might be essential for HCC development from cirrhosis, after HBV integration in the TERT promoter, while estrogen and its receptor had inverse actions [7, 24, 37].