We found CRKL promotes HCC hepatocarcinogenesis through enhancing cancer cells’ glucose metabolism via increasing GLUT1 expression, potentiating HKII activity and inactivating GSK3β activity, in the future, we hope the targeted‐CRKL drug will be designed to effectively inhibit glucose metabolism via increasing GLUT1 expression, potentiating HKII activity and inactivating GSK3β activity, which provides fundamental sight of molecule‐targeted therapy of cancer, molecule‐targeted therapy will represent the future development direction of treatment of tumours. This evidence concerns the gene GSK3B and neoplasm.