Together these results suggest that conventional chemotherapeutic agents, including anthracyclines and taxanes, induces FOXK2 to accumulate in the nucleus, where it induces the expression of downstream targets, including FOXO3a, a crucial mediator of the cytotoxic and cytostatic actions of anticancer chemotherapeutic agents in breast cancer cells13, 15 (Supplementary Figure S13). This evidence concerns the gene FOXK2 and breast carcinoma.