In light of recent renewed interest in studying altered metabolism in cancer [28] owing to IDH1/2 somatic mutations in AML and GBM, the compound effects of single genomic events on metabolic and oncogenic pathways, suggest that disruption of metabolic pathways by somatic mutations may be more widespread than previously thought and provides an impetus for novel therapies that might restore normal metabolic function in a cancer-cell specific manner. This evidence concerns the gene IDH1 and acute myeloid leukemia.