The findings concerning PAH, even if significant, should be interpreted with caution because of the limited number of patients; nevertheless these results are consistent with the assumption that the exact role of IL-17A in the pathogenesis of fibrosis is complex, and it would have rather a modulatory function than a definite pro-fibrotic or anti-fibrotic effect, depending on different tissues, disease stage and interaction with other cytokines that regulate fibrosis and vascular damage. The gene discussed is IL17A; the disease is pulmonary arterial hypertension.