100% of patients with KMT2A rearrangements (N=7), and 50% of patients with extra-medullary AML (N=4) achieved a CRc. In R/R AML, mutations in tumor suppressor (TS) genes (TP53, WT1, PHF6) were more frequently identified in patients without response (66% vs. 19%, p-value: 0.014) while 100% of R/R patients with NPM1 mutated AML achieved CRc.