According to the Canadian Cancer Society, one in nine women will develop breast cancer within their lifetimes, and one in 27 will die from it. Unfortunately, the current treatment option of metastatic breast cancer--taxane based chemotherapy--has substantial shortcomings. We rationalized that understanding the mechanisms of taxane cytotoxicity could lead to improved anti-cancer treatment options. With this objective in mind, we have identified that elevated levels of the protein, Bad, was a strong and independent prognostic factor for overall survival of breast cancer patients after adjuvant taxane chemotherapy. Mechanistically, this activity was independent of the well-documented ability of Bad to trigger the mitochondrial apoptotic machinery. Instead Bad facilitated cell death through stimulation of proliferation, thus sensitizing cells to taxane cytotoxicity. Our results elucidate a mechanism for taxane resistance, identify a clinically relevant prognostic marker for taxane treatment of breast cancer and highlight a new emerging non-apoptotic role for Bad.