Although aberrant TF expression is not restricted to specific AML subtypes [8,15,17], we and others showed that further mechanisms next to TF expression by PBMCs and shedding of TF-bearing MVs contribute to systemic coagulation activation in AML, including acquired activated protein C resistance and release of neutrophil extracellular traps (NETs) [8,17,72,73,74]. Here, TF is linked to acute myeloid leukemia.