We previously reported that in organoid-cultured bovine pulmonary arteries (BPA), pulmonary hypertension (PH) mediators hypoxia or endothelin-1 induced an increase in superoxide levels and deficiency of cartilage oligomeric matrix protein (COMP) affecting the bone morphogenetic protein receptor-2 (BMPR2) function [2,3]. This evidence concerns the gene BMPR2 and pulmonary hypertension.