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Progressive improvements in response and survival have mirrored these improvements in treatment options. Traditionally adverse subtypes such as\n                    <jats:italic>FLT3<\/jats:italic>\n                    \u2013internal tandem duplication\u2013positive AML now have better outcomes with potent FLT3 inhibitors, and menin inhibitors in\n                    <jats:italic>KMT2A<\/jats:italic>\n                    \u2010rearranged and other MEIS\/HOX\u2013dependent leukemias hold promise toward improving outcomes. More patients with AML are now able to undergo a consolidative allogeneic hematopoietic stem cell transplantation (HSCT), and the rates of nonrelapse mortality with or without HSCT have also decreased. Comprehensive genomic interrogation of AML has elucidated mechanisms of response and resistance to treatments, which has enabled more precise decision algorithms and better prognostication. Deep levels of measurable residual disease assessment in some AML subsets hold the potential to dynamically modify treatment on the basis of these responses. Improving frontline intensive and low\u2010intensity therapies, by incorporating venetoclax and other targeted agents, is the most important intervention to improve AML outcomes. Despite these developments, a sizeable percentage of AML, such as AML with\n                    <jats:italic>TP53<\/jats:italic>\n                    or\n                    <jats:italic>MECOM<\/jats:italic>\n                    aberrations, postmyeloproliferative neoplasm AML, and so forth, remains as subsets without significant improvement in outcomes and no targeted options. Evolving strategies with natural killer cell\u2013based approaches, novel antibody\u2013drug conjugates, bispecific T\u2010cell engagers, and engineered chimeric antigen receptor T\u2010cell therapies are being evaluated, and may fill the therapeutic vacuum for some of the high\u2010risk AML subtypes.\n                  <\/jats:p>","DOI":"10.1002\/cncr.35806","type":"journal-article","created":{"date-parts":[[2025,3,19]],"date-time":"2025-03-19T12:29:39Z","timestamp":1742387379000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":28,"title":["Therapeutic horizon of acute myeloid leukemia: Success, optimism, and challenges"],"prefix":"10.1002","volume":"131","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6831-2567","authenticated-orcid":false,"given":"Jayastu","family":"Senapati","sequence":"first","affiliation":[{"name":"Department of Leukemia The University of Texas MD Anderson Cancer Center  Houston Texas 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