Previous investigations revealed that disruption of BCATm resulted in increased energy expenditure and alterations in complex 1 of the mammalian target of rapamycin (mTORC1) and the AMP-regulated protein kinase (AMPK) in the heart, liver, and skeletal muscles.25,35 To test whether tumours isolated from BCATmKO mice fed standard rodent chow would show changes in mTORC1 signalling and AMPK, we measured the phosphorylation of S6, one of the downstream targets of mTORC1, as well as the total and phosphorylated forms of AMPKα in tumour tissues of BCATmKO and WT mice. This evidence concerns the gene MTOR and neoplasm.