Many inflammatory mediators [prostaglandin E1 (PGE1), PGE2, TNF-α, IL-1, IL-6, IL-8, nitric oxide, and platelet-activating factor], and pathophysiological conditions (hypoxia, pulmonary hypertension) have been shown to induce the expression of VEGF, angiogenesis, or both [30,31]. This evidence concerns the gene VEGFA and pulmonary hypertension.