Osteoblast deletion of Foxo1 prevented Ctnnb1CAosb‐driven AML development as evidenced by a lack of blasts and neutrophils with nuclear hypersegmentation in the blood, as well as blast infiltration of liver at periportal sites; this type of liver infiltration is commonly observed in murine AML models driven by active beta‐catenin and fusion proteins AML1/MDS1/EVI [63, 65]. The gene discussed is FOXO1; the disease is acute myeloid leukemia.