BCAT1 and neoplasm: Studies have found that in TKI-resistant cells, upregulated BCAT1 reprograms BCAA metabolism and promotes α-ketoglutarate (α-KG)-dependent demethylation of histone H3 at lysine 27 (H3K27), leading to the de-repression of glycolysis-related genes, thereby enhancing glycolysis and promoting tumor progression.