Importantly, similar to myofibroblasts, the very same Class-I and Class-II HDACs were also found to be upregulated in abnormal “proliferative” KRT5+ bronchiolar basal cells covering fibroblast foci, distal airspaces and honeycomb cysts in IPF lungs, whereas proSP-C+ AECII revealed a marked lack of many HDAC enzymes, suggesting that HDACs may govern the aberrant bronchiolization process of distal alveoli in IPF as well [165,174]. This evidence concerns the gene KRT5 and idiopathic pulmonary fibrosis.