Gao et al. continued their investigations by assessing the role played by reactive oxygen species (ROS) in the antitumor activity of CDDO-Me against OVCAR-5 and MDAH-2774 ovarian cancer cells (111); the authors revealed that CDDO-Me has the ability to generate ROS (hydrogen peroxide, H2O2) and that pre-treatment with N-acetylcysteine not only inhibited ROS generation but prevented or even blocked all previously mentioned anticancer mechanisms induced by CDDO-Me, in particular the down-regulation of the AKT/NF-κB/mTOR signaling pathway. This evidence concerns the gene MTOR and ovarian carcinoma.