HDAC8 and pulmonary fibrosis: Regarding the final member of Class I HDACs, HDAC8, limited studies have been published in the last five years with regards to IPF, though it was previously established that HDAC8 expression is increased in IPF lung tissue and NCC170, an HDAC8 inhibitor was able to attenuate pulmonary fibrosis in bleomycin-injected mice [26].