Namely, neuraminidase 1(NEU1)-deficient fibroblasts cells, which share the phenotype of myofibroblast, can secrete numerous EVs loaded with activated components of the transforming growth factor (TGF)-β and WNT signaling pathways and induce fibrotic features in normal fibroblasts [58], indicating that the down regulation of NEU1 in IPF may be responsible for the overexpression of EVs and activation of profibrotic signals cascade. This evidence concerns the gene TGFB1 and idiopathic pulmonary fibrosis.