A comparison of an anti-fibrotic efficacy of several PDE4 inhibitors to the two therapies approved by Food and Drug Administration (FDA) for idiopathic pulmonary fibrosis (pirfenidone and nintedanib) showed an equivalent reduction in the lung fibrosis with PDE4 inhibitors to pirfenidone and nintedanib, with a decrease in plasma levels of surfactant protein SP-D and of several chemokines implicated in lung fibrosis, and an in vitro inhibition of fibroblast profibrotic gene expression [116]. The gene discussed is PDE4A; the disease is idiopathic pulmonary fibrosis.