CDKN2A and hepatocellular carcinoma: Bmi1 at least partially regulates cell cycle progression through the transcriptional regulation of the p16Ink4a.34, 35 Silencing of p16Ink4a expression has been implicated as a key event in HCC progression36, 37 and it has been reported that Bmi1 collaborates with c-Myc in lymphoma tumorigenesis via p16Ink4a.35 In the present study, we found that forced expression of Bmi1 in HPCs led to the downregulation of p16Ink4a.