RHEBP1 and acute myeloid leukemia: Interestingly, the phosphorylation level of S6 and 4E-BP1 in Rheb1Δ/Δ GFP+ cells were further decreased after rapamycin treatment compared with the control (Fig. 5f), indicating that Rheb1 is partially responsible for mTORC1 signaling in AML cells.