Additionally, the activation of molecular pathways and morphological changes, such as uncoupled endothelial nitric oxide synthase (eNOS), pro-inflammatory cytokines such as interleukin 1 and 6 (IL-1 and IL-6), and oxidative stress, among others, lead to pulmonary arterial remodeling and ultimately definitive pulmonary hypertension (PH) [11,12]. The gene discussed is NOS3; the disease is pulmonary hypertension.