Prior reports by our group have demonstrated that crisantaspase treatment diminishes protein synthesis in AML by interfering with cap-dependent mRNA translation downstream of mammalian target of rapamycin (mTOR) signaling, specifically by inhibiting the phosphorylation of p70 ribosomal S6 kinase (p70S6K), a key downstream effector of mTOR (6, 7). The gene discussed is MTOR; the disease is acute myeloid leukemia.