Our data are most consistent with the concept, as illustrated in Fig. 7, that SIK2 functions to suppress the malignant phenotypes of GC by inhibition of autophagy‐mediated degradation of protein phosphatases PP2A and PHLPP2 via mTORC1 signaling, thus inactivating AKT/GSK3β/β‐catenin signaling primarily owing to increased dephosphorylation of AKT. This evidence concerns the gene AKT1 and gastric cancer.