As an example, targeting oncostatin M (OSM), a member of the IL-6 cytokine family highly expressed in renal tissue of LN mice, improved tubulointerstitial fibrosis with increase expression of E-cadherin and decrease of mesenchymal markers such as α-SMA, fibronectin (FN) and Stat1/Stat3, indicating that OSM may activate EMT via the Jak-Stat signaling pathway [215]. This evidence concerns the gene OSM and lobular neoplasia.