Our findings are consistent with those of previous studies, which reported that the activation of GSK-3β via the inactivation of Akt inhibits the translocation of β-catenin from the cytoplasm to the nucleus, suggesting that combination treatment of DIM and 5-Fu inhibits Akt activity, which activates GSK-3β and thereby induces the degradation of β-catenin in GC cells. This evidence concerns the gene AKT1 and gastric cancer.