For example, coagulation abnormalities in high-risk patients with APL treated with ATRA were shown to be amenable to treatment via suppression of intrinsic mechanisms that accelerated extracellular chromatin degradation.30 Hamed et al.31 reported that ATRA, by upregulating thrombomodulin (TM) expression on the surfaces of endothelial cells and causing oscillatory elevation of TM expression on endothelial cells during ATRA treatment, played a role in the treatment of coagulation disorders in cancer patients. Here, THBD is linked to acute promyelocytic leukemia.