Furthermore, LBH589 inhibits HDACs and inactivates HDAC1 and HDAC2 via significant proteolysis, which abrogates profibrotic STAT3 phosphorylation and activates downstream signaling pathways, consequently decreasing cell proliferation, survivin expression, and the expression of genes associated with extracellular matrix (ECM) in IPF fibroblasts (Korfei et al., 2018). This evidence concerns the gene HDAC2 and idiopathic pulmonary fibrosis.