Moreover, it has been shown that heterozygous Bmpr2+/− mice have increased S. mansoni egg translocation in the lungs via enlarged hepatic sinusoids (34), and Bmpr2+R899X loss-of-function mutant mice develop “spontaneous” PH, reinforcing the crucial role of this signaling pathway in the development of PAH, including the infectious disease (35). This evidence concerns the gene BMPR2 and pulmonary arterial hypertension.