Conversely, Flt3ITD/+ disrupts LT-HSC quiescence, resulting in depletion of this compartment, and failure to develop acute leukemia in the absence of cooperating mutations.[12, 13, 18] We hypothesized that enhanced self-renewal and expansion in the LT-HSC compartment conferred by Dnmt3a deletion might “rescue” the LT-HSC depletion seen in Flt3ITD/+ mice, thereby increasing this primitive pool and the opportunity for additional mutations necessary to drive either myeloid or T cell leukemia to develop. The gene discussed is DNMT3A; the disease is T-cell leukemia.