In addition, by transfecting of ectopic PLK1 WT, PLK1 T210D into RGCC wild type and endogenous PLK1 knockout tumor cells, activation of AMPKα2 (p-AMPKα2) could be detected; however, transfection of ectopic PLK1 T210A into RGCC wild type and endogenous PLK1 knockout cells had a markedly reduced AMPKα2 phosphorylation level (Fig. S4I). The gene discussed is PRKAA2; the disease is neoplasm.