The central role of PLK isoenzymes in tumorigenesis has been emphasised lately by studies showing that PLK1 inhibition, either by antisense or siRNA, leads to dramatic antiproliferative effects on tumour cells in vitro (Spänkuch-Schmitt et al, 2002a, 2002b; Elez et al, 2003; Liu and Erikson, 2003), pointing at a potential therapeutic use of inhibitory strategies targeting PLK isoenzymes. The gene discussed is PLK1; the disease is neoplasm.