Our research team was the first to prove the involvement of EMT type 2 in pulmonary fibrosis related to HP, showing down-regulation of epithelial markers (Cdh1/E-cadherin, Ocln/Occludin, Cldn1, Jup) with simultaneous up-regulation of mesenchymal markers (Acta2/α-SMA, Cdh2/N-cadherin, Fn1/Fibronectin, Vim/Vimentin) supported by elevated levels of EMT-transcription factors (Snai1/Snail, Snail2, Zeb1/ZEB1, Zeb2/ZEB2, Nfkb/NFκB, Tgfb1/TGFβ, Ctnnd1/β-catenin) [53,54]. This evidence concerns the gene CLDN1 and hypersensitivity pneumonitis.