The latter tumor shows DNA cytosine hypermethylation, especially at the level of tumor-suppressor genes, that has been attributed to low expression of L-2-hydroxyglutarate dehydrogenase (L2HGDH) with consequent overproduction of the 2HG oncometabolite (the L isoform) that in turn causes functional inactivation of TET2. Here, L2HGDH is linked to neoplasm.