Given that PLK2–PLK1 interaction at prometaphase was mediated by PLK2 kinase domain, it is tantalizing to speculate that PLK2 may phosphorylate PLK1 to regulate cell-cycle progression in normal mammalian epithelial cells and that loss of PLK2 may change PLK1 subcellular location and cell cycle–dependent activity, thereby leading to a mitotic catastrophe and promoting tumor growth. The gene discussed is PLK2; the disease is neoplasm.