This observation is supported by our previous findings that interactions between G9a-mediated H3K9 methylation and histone deacetylation are critically involved in the repression of IP-10 in IPF (24) and suggests that similar epigenetic deregulation may account for the silencing of a group of antifibrotic genes in IPF. Here, CXCL10 is linked to idiopathic pulmonary fibrosis.