In addition, the phosphorylation level of AKT was significantly higher in ARID1A-deficient gastric cancer cells than in non-deficient cells, as well as frequent mutations in the PI3K/AKT signaling pathway (deletion of PTEN or activation of PIK3CA) in endometrial carcinomas with deficient ARID1A expression (53). This evidence concerns the gene ARID1A and gastric cancer.