Since pulmonary microvascular occlusion would be expected to involve both myeloid cell and HIF response, and given that occlusive venous thrombosis leads to the upregulation of HIF1α and HIF2α in myeloid cells [9,13], we next examined the impact of both myeloid HIF1α and myeloid HIF2α in a mouse model of thrombosis-associated pulmonary tumorigenesis [14]. This evidence concerns the gene HIF1A and deep vein thrombosis.