As tumours accelerating tryptophan catabolism still contain sufficient levels of tryptophan (57–59), it is likely that tumoural tryptophan levels cannot reach levels sufficiently low to activate the stress response pathways to low amino acid levels such as the general control non-derepressible-2 (GCN2) and the mammalian target of rapamycin (mTOR) (Figure 1). Here, MTOR is linked to neoplasm.