Mutant IDH1 produces the oncometabolite 2HG, which drives tumorigenesis in low-grade gliomas. One potential therapeutic option for such gliomas is treatment with a PI3K/mTOR inhibitor. Using cell models genetically-engineered to express mutant IDH1, we observed that PI3K/mTOR inhibition induced a reduction in 2HG levels in treated cells and tumors, that was associated with reduced cell proliferation and enhanced animal survival. The drop in 2HG was due to a reduction in its synthesis from both glucose and glutamine. Our study identifies MRS-detectable metabolic alterations that could serve as indicators of response for mutant IDH1 glioma patients undergoing treatment with PI3K/mTOR inhibitors.