Indirect evidence for the tumor-promoting effect of overexpressed PLK1 in (relapsed) ovarian cancer comes from the induction of synthetic lethality in a patient-derived ovarian cancer cell culture [274] and from the clinically approved antitumor effect of the PLK1 inhibitor B16727 (Volasertib®) [275]. The gene discussed is PLK1; the disease is ovarian carcinoma.