In particular, Sargsyan et al. demonstrated that SAA levels were correlated to increased endothelin-1 (ET-1) titers (r = 0.459, p = 0001) in 30 FMF patients affected by coronary heart disease, pulmonary hypertension, stroke, vasculitis (polyarteritis nodosa, IgA vasculitis, livedoid vasculopathy) and Raynaud’s phenomenon, compared to non-vasculopathic FMF patients and healthy controls, concluding that SAA may also represent a surrogate marker of endothelial injury [33]. The gene discussed is SAA2; the disease is pulmonary arterial hypertension.