While the nature of the decrease in CD34+ telocyte number and how this contributes to the development of fibrosis remain unclear, these cells have been suggested to counteract fibrosis by HGF-mediated inhibition of the TGF-β1/Smad signaling pathway in the rat model of renal fibrosis (Zheng et al., 2018) and by enhancing mesenchymal to epithelial transition during the process of decidualization in endometrium (Zhang F.-L. This evidence concerns the gene CD34 and renal fibrosis.