Several molecular and cellular mechanisms are involved in the pathogenesis of AML-associated coagulopathy, including AML cell expression of procoagulant proteins, exposure of procoagulant lipids, release of inflammatory cytokines (e.g., IL1β and TNFα) and microparticles and the adhesion to vascular cells, leading to activation of the coagulation cascade, platelets and endothelial cells [256]. This evidence concerns the gene IL1B and acute myeloid leukemia.