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. This evidence concerns the gene CDKN2A and lymphoma.