Importantly, inhibition of KDM6B restored H3K27me3 levels in Asxl1Y588XTg Kdm6bΔ/+ BM cells, prompting us to initiate preclinical studies to determine whether targeting KDM6B could potentially benefit patients with ASXL1 mutation–associated myeloid malignancies. The gene discussed is KDM6B; the disease is myeloid neoplasm.