Having observed that (i) PegC, a long-acting Erwinia chrysanthemi asparaginase, regulates p90RSK2 expression, (ii) asparaginases negatively impact the mTOR/p70RSK1 (p70S6K) pathway [13], (iii) ribosomal S6 kinase activity seems altered from GO-molecular functions enrichment analysis in all three treatments, and (iv) enhancement of anti-AML activity of Ven by PegC, we hypothesized that co-treatment with Ven and PegC significantly diminishes cellular protein synthesis through interference with active cap-mRNA translation downstream of mTOR signaling (Fig. 5a). This evidence concerns the gene RPS6KB1 and acute myeloid leukemia.