There is compelling evidence that reactive oxygen species (ROS) generation regulates a network of intracellular signals that may have negative consequences, such as cellular damage and aberrant physiological processes. Commonly, the term “oxidative stress” relates to a shift in redox status, for instance, an instability in the proportions of antioxidant enzymes. A thorough literature review was conducted across PubMed, Scopus, Web of Science, and Google Scholar, focusing on oxidative stress, leukemia biology, and ROS-targeted therapies. Data from studies published from 2006 to 2026 were prioritized, and important landmark studies were included for scientific context. Acute and chronic leukemogenesis, among other hematological cancers, have been linked to oxidative stress. High rates of hematopoietic blast cell proliferation and aberrant differentiation are characteristic of leukemogenesis in acute myeloid leukemia. Hyperleukocytosis, medullary illness, and aberrant thrombosis are all linked to this aberrant expansion and differentiation of blast cells. It is necessary to examine the molecular pathways underlying the onset, progression, and evolution of leukemogenesis driven by oxidative stress. Therefore, a thorough understanding of ROS production in leukemia can open new avenues for efficient therapeutic interventions, such as chemical, radiation, immunological, and targeted therapies targeting oncogenes and tumor suppressor genes. These diverse potential treatments aim to prevent leukemia recurrence and progression by targeting signal transduction pathways. This article discusses current research on the putative role in leukemia etiology, prospective treatments, and clinical trials that specifically target redox status in cancer.