Thus, in the absence of p16/p14, cyclin D/cdk4 activity is elevated, leading to Rb1 phosphorylation and E2Fs accumulation.17, 38 Besides, there are some studies reported that inactivation of the p16INK4A gene, owing to several reasons including allelic deletions of this locus and/or hypermethylation of p16/14 promoter, was found in HCCs.39, 40, 41, 42 In this study, we found that overexpression and decreased expression of Linc00441 may inversely regulate the G1 phase arrest and HCC cell lines proliferation in vitro and in vivo. Here, RB1 is linked to hepatocellular carcinoma.