The observed eminent lack of Class I HDACs in proSP-C+ expressing AECII in IPF is not only plausible due to increased alveolar ER stress and apoptosis but also considerably mirrored by increased p53-p21CIP1 activation and senescence in IPF-AECII, which has been widely reported by many scientists [17,118,119,120]. This evidence concerns the gene TP53 and idiopathic pulmonary fibrosis.