A similar approach in mice carrying both NRAS and EZH2 mutations showed that the hyperactivation of branched-chain amino acid (BCAA) metabolism due to the aberrant activation of BCAT1 was responsible for more aggressive MPNs with rapid progression to the acute leukemia phase, suggesting dietary BCAA restriction or the use of BCAT1 inhibitors in EZH2-mutated myeloid neoplasms [131]. This evidence concerns the gene BCAT1 and myeloid neoplasm.