Anti-fibrotic drugs such as pirfenidone and nintedanib inhibit the pro-fibrotic M2 phenotype in experimental models of lung fibrosis [41,42,96], and specific MEK-inhibitor and HDAC-inhibitor drugs were reported to inhibit M2 polarization in an experimental model of wet macular degeneration [97]. This evidence concerns the gene HDAC9 and pulmonary fibrosis.