Meanwhile, in the MPN-to-leukemia transformation (and possibly AML cases presenting with activating RAS mutations and EZH2-deficiency), activated BCAT1 cooperates with increased Gln uptake to enhance BCKA reamination, leading to increased BCAAs and mTORC1 signaling (Figure 2). The gene discussed is EZH2; the disease is acute myeloid leukemia.