Indeed, Finkin et al. hypothesized that loss of FBXW7/hCDC4 might have important effects on how cells respond to chemotherapeutic drugs, and showed that exposure of cells lacking FBXW7/hCDC4 to spindle toxins, such as taxol, commonly used in breast cancer treatment, renders cells more susceptible to endoreduplication and polyploidy [48]. The gene discussed is FBXW7; the disease is breast cancer.