FAS and pulmonary fibrosis: However, cell surface expression of Fas has also been reported to be regulated by post-translational mechanisms,4 and these mechanisms can be regulated by oxidative stress.40 Furthermore, fibroblast expression of FasL has been shown to promote epithelial cell apoptosis, which is also considered critical to the pathogenesis of IPF.41, 42 Whether FasL expression is regulated by histone modifications in pulmonary fibrosis is unknown.