In fact, association of overexpressed uPAR and beta1 integrins regulates two opposite pathways, activating ERK and inhibiting p38MAPKs, thus stimulating in vivo growth of carcinoma cells [91]; EGFR, which can associate with uPAR on the cell membrane, mediates the uPAR/integrin/fibronectin induced growth pathway [39]. This evidence concerns the gene EGFR and carcinoma.