There is growing evidence supporting the hypothesis of hypoxia-induced vasoconstriction that ultimately leads to pulmonary hypertension, which in turn may increase parietal RV stress in patients with extensive pulmonary lesions, thereby causing an increased NT-proBNP release from cardiomyocytes, a very plausible mechanism in the context of COVID-19 [168,169,170]. This evidence concerns the gene NPPB and pulmonary arterial hypertension.