HDAC6 deacetylates non-histone proteins like α-tubulin, and inhibiting it with compounds like trichostatin or tobramycin reduces TGF-β signaling and improves bleomycin-induced fibrosis in mice, suggesting that aberrant deacetylation in IPF AMs promotes fibrogenesis by enabling persistent activation of TGF-β target genes or by suppressing antifibrotic genes [100,102]. Here, HDAC6 is linked to idiopathic pulmonary fibrosis.