As the role of PARPi is being explored in clinical trials for AML subtypes (RUNX1-RUNX1T1 and PML-RARα fusions, FLT3- and IDH1-mutated), a shorter course of therapy with those agents to achieve synergy with chemotherapy in the upfront treatment of leukemia may have a different risk profile than prolonged use as a solid tumor maintenance therapy. The gene discussed is FLT3; the disease is acute myeloid leukemia.