In vivo studies further revealed that MDSCs lost their immunosuppressive function after artemisinin intervention and activated T-cell function by increasing iNOS expression and thereby activating T-cell function [88]the core mechanism of which was related to the activation of the PI3K/AKT, mTOR, and MAPK pathways, which promotes the reprogramming process of functional polarization of MDSCs, which may provide a new therapeutic strategy for enhancing anti-PD-L1 cancer immunotherapy. The gene discussed is AKT1; the disease is cancer.