They facilitated the dephosphorylationof the hyperactivated Overactivation of the phosphatidylinositol 3-kinase/proteinkinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathway,increased reactive oxygen species (ROS) production, and facilitatedthe conversion of M2 macrophages to M1 macrophages.263 These findings suggest a promising strategy for combatingcisplatin-resistant ovarian cancer and may provide a treatment optionfor other cisplatin-resistant tumor types. This evidence concerns the gene MTOR and ovarian cancer.