The primary mechanism was that in the BCAA-BCAT1-αKG pathway, BCAT1 stabilized the α protein required for the maintenance of LSCs by regulating the level of intracellular α-KG, limited the activity of α-KG-dependent Recombinant Egl Nine Homolog 1 (EGLN1), reduced the activity of tet methylcytosine dioxygenase 2 (Tet2), these various oncogenic drivers were all designed to promote the rapid growth of malignant tumors (42). This evidence concerns the gene BCAT1 and cancer.