Abnormal WNT/β-catenin signaling mediated the activation of KIF2C, which subsequently antagonized TBC1D7 and destabilized the TSC complex, resulting in the abolishment of TSC2 suppressive efficiency on mTORC1 signaling transduction, thereby activating the mTORC1 signaling and promoting the development of HCC [107]. This evidence concerns the gene KIF2C and hepatocellular carcinoma.