In chronic myeloid leukemia (CML), BCAT1 is aberrantly activated and required for tumor propagation by promoting BCAA production.13 Also, BCAT1 is reported to cooperate with NRAS G12D to sustain intracellular BCAA pools and promote leukemic transformation through activated mTOR signaling.33 In our study, we demonstrated that BCAT1 facilitated BCAA anabolic metabolism, thereby enhancing α-KG-dependent glycolysis to orchestrate resistance to third-generation EGFR TKIs in NSCLC. This evidence concerns the gene BCAT1 and neoplasm.