In this context, we hypothesized that chemerin (alone or in association with other factors already known to be implicated in the pathogenesis of pulmonary hypertension) may influence pulmonary artery SMC proliferation, apoptosis, and migration, which are crucial to the pathophysiological development of pulmonary artery remodeling observed in pulmonary hypertensive diseases. The gene discussed is RARRES2; the disease is pulmonary hypertension.