Herein, we found that overexpression of AGK enhanced the resistance of HCC cells to cisplatin-induced apoptosis, whereas silencing AGK increased the sensitivity of HCC cells to cisplatin-induced apoptosis; these effects were mediated via modulation of the expression of multiple anti-apoptotic factors including c-FLIP, XIAP, Bcl-xl and Bcl-2. This evidence concerns the gene BCL2 and hepatocellular carcinoma.