Wang et al. reported that Ac-SDKP administration played a therapeutic role in pulmonary fibrosis by downregulating histone deacetylase family member 6 (HDAC6) and reversed the reduced expression of α-tubulin acetyltransferase 1 (α-TAT1) in silicosis disease rat model and primary rat lung fibroblasts treated by Ang II to stabilize α-Ac-Tub expression level, resulting in inhibition of myofibroblast differentiation and collagen generation [130]. This evidence concerns the gene ATAT1 and pulmonary fibrosis.