They reveal that synthetic lethality could be generated by combining paclitaxel with BIBF1120 (an investigational VEGFR, PDGFR, and FGFR multityrosine kinase inhibitor with established antiangiogenic activity), which together abrogated the G2/M checkpoint in p53-null endometrial cancer cells via modulation of G2/M checkpoint regulators followed by induction of mitotic cell death. The gene discussed is TP53; the disease is endometrial cancer.