AKT1 and cancer: The cell-cell junctions formed by interaction between p120ctn and E-cadherin are critical in maintaining normal esophageal epithelial homeostasis; however, p120ctn expression in the ESCC TME is decreased or absent, leading to E-cadherin degradation and NF-κB, AKT, and STAT3 phosphorylation in cancer cells, promoting cancer cell GM-CSF release, which can recruit MDSCs into the TME.