HDAC9 and idiopathic pulmonary fibrosis: Taken together, we suggest that in IPF, repetitive AEC injury in a (genetically susceptible) ageing individual leads to abnormal HDAC overexpression and HDAC-mediated epigenetic reprogramming in lung fibroblasts as well as bronchiolar basal cells, resulting in excessive production of profibrotic mediators, persistent AECII injury, progressive bronchiolisation, and the ongoing activation and persistence of lung fibroblasts/myofibroblasts.