Importantly, in contrast to myofibroblasts and basal cells, expression of many HDACs appeared to be sparse or even absent in IPF-AECII undergoing proapoptotic ER stress [165], which is in agreement with the degradation and depletion of many HDAC enzymes under conditions of severe ER/oxidative stress or apoptosis [267,268,269,270,271]. The gene discussed is HDAC9; the disease is idiopathic pulmonary fibrosis.