STAT3 and idiopathic pulmonary fibrosis: In agreement with these findings, it could be demonstrated that panobinostat abrogated STAT3-phosphorylation at tyrosine 705 (Tyr705) and its fibrotic action in IPF fibroblasts, thus offering a plausible explanation for the reduction of survival- and ECM-associated genes in response to global HDAC inhibition and evidence for the involvement of HDACs in increased expression of such profibrotic genes [249].