We will examine whether there are distinct genetic alterations in AML cells of AML patients with activated β-catenin signaling in osteoblasts that facilitate the progression of disease. For this purpose we will compare the somatic genetic alterations in AML cells of 16 patients who present osteoblast involvement by activated β-catenin signaling to 34 AML patients that do not present it through Sanger sequecing. Our goal is to identify correlating mutational signatures between stromal and AML cells upon activated osteoblastic β-catenin signaling.