Recent cancer genomic data revealed that different somatic mutations of metabolic genes in different cancer types such as loss of function of mutated succinate dehydrogenase (SDH) or fumarate hydratase (FH) in certain renal cell carcinomas and mutated isocitrate dehydrogenase (IDH) 1 or 2 in glioma, acute myeloid leukemias, chondrosarcomas, and amplification of phosphoglycerate dehydrogenase (PHGDH) in estrogen receptor (ER)-negative breast cancer and melanoma further suggest that somatic alterations in metabolism could satisfy cancer-specific demands for fueling tumor growth [12–16]. The gene discussed is FH; the disease is acute myeloid leukemia.