Exploring Experimental Hematology: June 2021 (Volume 98)
![Image](https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiDIPJxhYrulcA-g87A12EtoRMtiurlLTEfGirUHiny9ub0UkiPk44iHvWKHiKVjfB2dw9fdYYH8iPGXWeWB6cIQoCGFcRUftc8rPSs3pX0qNDFx2oi5sTMKHgbW3FUXK2YrcaNDz5CP1rCopBYVTZGCTTa9k_mzINautYRwhqeOJtPWDykf5ZLHp2okQ/w640-h205/Exploring%20ExpHem.png)
DNA methylation therapy joins forces in IDH2 -mutant AML Isocitrate dehydrogenases 1 and 2 ( IDH1 /2) are frequently mutated in Acute Myeloid Leukemia (AML), with nearly 20% of patients carrying gain-of-function point mutations in these genes (Ley et al., 2013) . IDH2 is a metabolic enzyme that catalyzes the conversion of isocitrate to 2-oxoglutarate during the Krebs cycle. Patients carrying IDH2 gain-of-function mutations produce instead high levels of the oncometabolite 2-hydroxyglutarate (2-HG), which inhibits oxoglutarate-dependent enzymes such as the TET family of methylcytosine dioxygenases, responsible for active DNA demethylation (Xu et al., 2011) . As a consequence, IDH2 mutations in AML patients induce DNA hypermethylation and inhibit hematopoietic differentiation (Figueroa et al., 2010) . Azacytidine (AZA) and enasidenib (ENA) are commonly used AML therapies which induce DNA hypomethylation, albeit through different mechanisms. AZA is a nucleoside analog that inhibits