Although there is no direct research proving that HDAC7 plays a role in PF, existing studies have shown that in LPS-stimulated macrophages and in mouse models, HDAC7 binds to the TRAF6-TAK1 complex through a non-enzymatic mechanism, activating the MAPK/NF-κB pathway, promoting the secretion of pro-inflammatory factors such as IL-6 and TNF-α, and providing an inflammatory microenvironment for fibrosis [72]. This evidence concerns the gene HDAC7 and pemphigus foliaceus.