The increased growth with increased BCAT1 expression in CML could be explained by elevated BCAA concentrations, particularly leucine, resulting in activation of the mTORC1 pathway.15 Similar observations have been made in human hepatocellular carcinomas and animal models of liver cancer.52 However, in A11 cells knockdown of BCAT1 and in S2 cells increased BCAT1 expression had no effect on mTORC1 activity, as evidenced by the absence of a change in phospho-S6 concentration. Here, BCAT1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.