These modifications can appear due to the fact that SARS-CoV-2 infection can trigger systemic inflammation, through a “cytokine storm” (possibly through the stimulated Weibel-Palade body ET-1 secretory pathway [42]), accumulation of angiotensin-II by downregulating the angiotensin converting enzyme 2, systemic thromboembolic disorders, and even pulmonary arterial hypertension, all leading to elevations of ET-1 [4]. The gene discussed is EDN1; the disease is pulmonary arterial hypertension.