AKT1 and neoplasm: In various tumor mouse models (such as lung cancer, breast cancer and colon cancer), it has been found that the tumor-derived factor GM-CSF induces miR-200c overexpression to activate Akt by negatively regulating the transcriptional regulator friend of Gata 2 (FOG2) and PTEN expression, further enhancing the immunosuppressive activity of MDSCs (59) (Table 1).