Moreover, THY1 overexpression was recently shown to regulate the progression of acute interstitial pneumonia (AIP) by significantly decreasing the expression of profibrotic proteins such as Matrix Metallopeptidase 2 (MMP-2), Occludin, α-SMA, Vimentin and β-catenin, and phosphorylation levels of β-catenin, resulting in inhibition of the WNT signaling pathway, a critical pathway in the pathogenesis of IPF, resulting in decreased proliferation and increased apoptosis of lung fibroblasts [32]. This evidence concerns the gene VIM and idiopathic pulmonary fibrosis.