Histone deacetylase inhibition can also increase Fas expression, which exhibited low level expression in fibroblasts from both IPF patients and mice with experimental pulmonary fibrosis, and restore sensitivity to Fas-mediated apoptosis, indicating the key role of histone modification in the development of anti-apoptotic fibroblasts (59). The gene discussed is FAS; the disease is idiopathic pulmonary fibrosis.