Although nearly all Class I and Class II HDAC enzymes appeared to be actually absent in differentiated proSP-C+ IPF-AECII but abnormally upregulated in KRT5+ bronchiolar basal cells [165], it can be speculated that hyperplastic dedifferentiated AEC-like cells without proSP-C expression, as recently described as transitional KRT8+high progenitors in fibrotic lungs [301,309,310], might overexpress HDAC enzymes for their terminal differentiation into KRT5+ basal cells. The gene discussed is KRT8; the disease is idiopathic pulmonary fibrosis.