In chronic myeloid leukaemia (CML) increased BCAT1 expression drives progression by increasing the production of BCAAs15 whereas in acute myeloid leukaemia (AML) it drives proliferation by lowering the concentration of α-KG.5 Increased expression of BCAT1 has been observed in IDH wild-type glioblastoma, but not in gliomas harboring mutations in IDH1 and IDH2. Here, IDH2 is linked to central nervous system cancer.