Interestingly, the weak Class I inhibitor valproic acid (VPA) was also shown to efficiently reduce cell proliferation, surviving expression, collagen-I protein turnover in IPF fibroblasts, and these effects were accompanied by the significant degradation and loss of HDAC2 [165], an effect which has been observed in various cells upon VPA treatment [276]. Here, HDAC2 is linked to idiopathic pulmonary fibrosis.