The MAPK and/or AKT signalling pathways are constitutively active in the majority of AML cases.[12, 13] RpS6 is a downstream mediator of both pathways,[7, 8] and is constitutively phosphorylated in patient samples.[14] P-rpS6 has been used previously as a sensitive marker for mTORC1 activation in flow cytometric studies.[15, 17, 18] To examine basal phosphorylation and inhibitor-induced dephosphoryation of rpS6 in our assay system, we cultured MV4-11s for 4 hours with the mTORC1 inhibitor torin1, the ERK inhibitor U0126 and the akt inhibitor LY294002. The gene discussed is RPS6; the disease is acute myeloid leukemia.