Taken together, there are several compelling rationales for combining bevacizumab and temsirolimus in gynecologic tumors: i) temsirolimus inhibits mTOR and the PI3 kinase/AKT/mTOR pathway is critical in several gynecologic malignancies [24, 25]; ii) temsirolimus attenuates upregulation of HIF-1α levels, which may be a resistance mechanism for bevacizumab [21, 26]; iii) single-agent activity with temsirolimus and bevacizumab have been demonstrated in gynecologic cancers [27, 28]; and, iv) the two agents have non-overlapping toxicities. The gene discussed is MTOR; the disease is female reproductive organ cancer.