Inflammatory signaling in the niche itself has long been linked to AML progression and hematopoietic dysfunction [5–10], and several mechanisms and mediators have been proposed including NF-κB expression programs in AML blasts [11], as well as secretion of interleukin (IL)−6 [9] and IL-1β [12]. Here, NFKB1 is linked to acute myeloid leukemia.