Further, Class IIA HDAC4, which is prominently upregulated in IPF versus normal fibroblasts, was shown to form a protein complex with some cytoplasmic protein phosphatases (PP) in response to TGF-β to prevent the dephosphorylation and inhibition of AKT in fibrotic lung fibroblasts for inducing and maintaining AKT-mediated profibrotic gene expression [250]. Here, TGFB1 is linked to idiopathic pulmonary fibrosis.