Endothelial dysfunction and defective thrombus neovascularization accompanied by a decrease in the expression of factors involved in proliferative pathways of vascular cells, such as bone morphogenetic protein receptor type 2 (BMPR2) or TGF-β1, are thought to play a key role in the pathogenesis of CTEPH [3]. This evidence concerns the gene BMPR2 and chronic thromboembolic pulmonary hypertension.