Acute myeloid leukemia (AML) is a malignant disease of bone marrow stem cells that can be fatal with current treatment methods. The median age of patients is 68, and a substantial proportion of cases are attributable to geriatric patients. Following the administration of induction chemotherapy, complete remission (CR) is observed in approximately 73% - 45% of patients in the ELN-2022 favorable-adverse risk groups, respectively. However, overall survival (OS) and progression-free survival (PFS) are not satisfactory despite current treatments. The five-year PFS was estimated at 52% - 16%, and the five-year OS was 55% - 15%, respectively. As the pathogenesis of AML becomes clearer, clinical trials on current targeted therapies are increasing, and being developed to accompany or replace standard AML treatments that have been similar for nearly 50 years. It is now evident that epigenetic-based treatments can lead to significant changes in the fundamental model that underpins therapeutic interventions. The combination of BCL2 inhibitor venetoclax with hypomethylating agents has significantly improved survival, particularly in elderly and unfit patients. Studies are ongoing to combine intensive therapies with induction and consolidation therapy. Three FLT3 inhibitors (midostaurin, gilteritinib, and quizartinib) have shown promising results in induction and consolidation therapies, salvage therapies, and follow-up therapies after allogeneic transplantation. A phase Ib-II trial of crenolinib, a potent type I second-generation FLT3 inhibitor, demonstrates that its use with intensive therapy in newly diagnosed AML patients under 60 years of age improves survival and results in higher rates of MRD negativity. In addition, ongoing trials are also evaluating the 7 + 3 + midostaurin versus 7 + 3 with gilteritinib (NCT04027309). Other targeted studies are ongoing with IDH inhibitors (ivosidenib and olutasidenib targeting IDH1 mutations; enasidenib targeting IDH2 mutations). Olutasidenib has been shown to provide better response rates and survival compared to ivosidenib in elderly, unfit patients, and combination with azacitidine also increases OS. Other promising studies for AML appear to be focused on menin inhibitors. The phase 1 trial of Revumenib (AUGMENT-101 trial) and Ziftomenib (KOMET-001 trial) (both studies in patients with KMT2A rearranged and NPM1m R/R AML) have yielded positive results, and phase 2 trials are eagerly awaited. A phase 1 trial evaluating a third oral Menin inhibitor, JNJ-75276617, results rates were similar to the other 2 inhibitors. Clinical trials are now ongoing these drugs in combination with additional low dose and high dose chemotherapy regimens (NCT05735184, NCT05886049). Another area is immunotherapy in AML. The success of allogeneic stem cell transplantation has demonstrated the potential for immunotherapy. Talacotuzumab and Pivekimab, targeted to CD123, appear to be particularly effective in relapsed-refractory (R/R) patients, and combination studies with FLAG-IDA are ongoing. Additionally, Tagraxofusp, a drug containing IL-3 ligand conjugated to the first 388 amino acids of diphtheria toxin, has been studied combination with Azacitidine/Venetoclax in newly diagnosed AML patients. MRD negativity was found in 71% of patients. Magrolimab, which acts on CD47, has promising results in patients with R/R AML. The potential of ongoing targeted therapies to provide new insights into the treatment of AML.