Indeed, pirfenidone, one of the two currently US Food and Drug Administration (FDA) approved drugs (pirfenidone and nintedanib) for treatment of human IPF, exerts its anti-fibrotic property in part by suppressing TGF-β expression relevant to macrophage M2 polarization and fibroblast activation [121]. The gene discussed is TGFB1; the disease is idiopathic pulmonary fibrosis.