According to the results of the present study, it can be speculated that the high blood flow shear stress acted on the pulmonary artery endothelial cells, activating NF-κB signaling pathways and initiating gene transcription to produce vasoactive mediators, pulmonary vasoconstriction and pulmonary vascular remodeling, and thus leading to pulmonary hypertension. This evidence concerns the gene NFKB1 and pulmonary hypertension.