Recent renewed interest in BLVRB and the heme degradation pathway provides unique opportunities for further research, predicated on (1) initial studies in humans in which a redox mutation was causally associated with enhanced platelet counts in two distinct human disorders of thrombocytosis, additionally supported by (2) subsequent models of murine Blvrb deficiency that display comparable phenotypes of exaggerated proplatelet formation. This evidence concerns the gene BLVRB and Thrombocytosis.