A recent phase I study in which rapamycin was combined with MEC (mitoxantrone, etoposide, cytarabine) polychemotherapy failed to demonstrate any synergistic effect of the combination in relapsed/refractory AML patients, even if proof of rapamycin biological activity in vivo was detected, consisting in the dephosphorylation of p70S6K [134]. The gene discussed is RPS6KB1; the disease is acute myeloid leukemia.