Background: Acute myeloid leukemia (AML) is a highly fatal disease occurring due to the proliferation and accumulation of myeloid progenitor cells. Th17 cells had been claimed by many studies to play a role in the development of AML. Aim Of work: This work aimed to detect the possible role of IL 17 F and IL 23 gene polymorphisms in the pathogenesis of AML, relation to prognosis, and response to treatment. Subjects, materials, and methods: This study was done on 68 patients with newly diagnosed AML (as a patient group), together with 56 matched healthy volunteers (control group). IL 17 F and IL 23 gene polymorphisms were genotyped by real-time polymerase chain reaction (Real-time PCR). Results: No significant differences were detected between patients and controls in respect to   IL 17 genotype distribution, there were statistically significant differences between patients and controls regarding IL 23 genotype distribution. No statistically significant relation was found between interleukin 17 and interleukin 23 and any of the bad prognostic markers. Conclusion: We concluded that IL23 gene polymorphism could be considered an independent risk factor in the pathogenesis of AML, while we could not prove that IL 17 gene polymorphism has a role in the development of AML.