In contrast, STAT3 and AKT were not hyper-phosphorylated in Flt3ITD mutant HSC/MPPs or HPCs (Figure 4A and Figure 4—figure supplement 1A), and Rictor deletion (PI3K/mTORC2 pathway inactivation) did not rescue Flt3ITD-driven HSC depletion or MPN (Figure 4—figure supplement 1B,C). The gene discussed is STAT3; the disease is myeloproliferative neoplasm.