AKT1 and lung carcinoma: [120] Xiao and colleagues found that Dihydroartemisinin dose-dependently promotes M1 polarization of TAMs through modulation of the AKT/mTOR signaling pathway by increasing the expression of molecules related to the M1 phenotype while decreasing the expression of molecules related to the M2 phenotype; this in turn inhibits the growth of lung cancer.[121]