,84,85 The current view is that, in nascent tumor cells, elevated R-2-HG may dysregulate multiple enzymes, including some 2-OG-dependent dioxygenases and metabolic enzymes, leading to altered cellular metabolism presumed to support or promote tumorigenesis.86, 87, 88 In myeloid cancers, mutations in IDH1/2 are considered important for disease progression via similar mechanisms.85 Here, IDH1 is linked to neoplasm.