To investigate whether KIF18B promoted HCC progression through activating mTORC1 signaling, we treated KIF18B-depleted HCCLM3 cells with MHY1485, an agonist of mTORC1 signaling, and treated KIF18B overexpressing BEL-7402 cells with INK-128, an mTOR ATP site inhibitor. This evidence concerns the gene MTOR and hepatocellular carcinoma.