Transfection of ectopic PLK1 T210D (a hyper-phosphorylated PLK1 mutant), rather than PLK1 T210A (a hypo-phosphorylated PLK1 mutant), could restore AMPKα2 phosphorylation level in RGCC-deficient and endogenous PLK1 knockout tumor cells. This evidence concerns the gene PLK1 and neoplasm.