Illustration of mechanism and effects of ETosis in malignant promyelocytes following exposure to ATRA. Malignant promyelocytes on exposure to ATRA undergo nuclear and granule membrane breakdown. Subsequently, there is intermingling of chromatin and cytoplasmic contents within the cell. Following this, there is bulging, further weakening, and final breakdown of the cell membrane with release of promyelocytic chromatin, which forms a net-like structure and binds to other cells and endothelial cells. The surface of the extracellular chromatin, along with the surface membrane of the cell from which it arose, concentrates procoagulant factors and fibrin. The extracellular chromatin and cf-DNA also facilitate increased generation of plasmin and activate the intrinsic coagulation cascade. Promyelocytic extracellular chromatin also damages endothelial cells with which they come into contact, leading to a procoagulant phenotype, and provides additional surface area for clot formation and fibrin deposition. Ensuing endothelial cytotoxicity probably also leads to loss of endothelial cell integrity. RBC, red blood cell. Professional illustration by Somersault18:24.