It is intriguing that in mouse models, depletion or inactivation of 12-LOX prevents major disease development and/or progression, though it will be important to determine if there are deleterious global effects of inactivation of the 12-LOXs, as the Alox15 null mice show hematopoietic defects leading to a myeloproliferative disorder as well as defective erythropoiesis [147,148]. This evidence concerns the gene ALOX15 and myeloproliferative disorder.