We and others have reported that IPF-fibroblasts exhibit a cancer-like phenotype due to aberrant overexpression of class-I and class-II histone deacetylase (HDAC) enzymes, which appeared to be responsible for their abnormal activation and persistence in IPF, presumably as the result of alterations in the acetylation status of the chromatin and various non-histone proteins [31–33]. This evidence concerns the gene HDAC9 and idiopathic pulmonary fibrosis.