RON distribution is restricted to cells that have epithelial origin and studies have demonstrated that RON expression is required for attenuating the inflammatory response, controlling the macrophages activities during infections.166 RON overexpression was observed in cancers localized in pancreas, bladder, lung, breast, colon, thyroid and skin, its overexpression is correlated with advanced clinical stages, and it seems that RON can modulate cell growth and migration via MAPK/Akt pathways sustaining tumorigenicity.167–170. This evidence concerns the gene AKT1 and cancer.