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Acute myeloid leukemias (AMLs) comprise a group of genetically heterogeneous hematological malignancies that result in the abnormal growth of leukemic cells and halt the maturation process of normal hematopoietic stem cells. Despite using molecular and cytogenetic risk classification to guide treatment decisions, most AML patients survive for less than five years. A deeper comprehension of the disease’s biology and the use of new, targeted therapy approaches could potentially increase cure rates. RAS oncogene mutations are common in AML patients, being observed in about 15–20% of AML cases. Despite extensive efforts to find targeted therapy for RAS-mutated AMLs, no effective and tolerable RAS inhibitor has received approval for use against AMLs. The frequency of RAS mutations increases in the context of AMLs’ chemoresistance; thus, novel anti-RAS strategies to overcome drug resistance and improve patients’ therapy responses and overall survival are the need of the hour. In this article, we aim to update the current knowledge on the role of RAS mutations and anti-RAS strategies in AML treatments.