In this process, lysyl oxidase-mediated cross-linking of the tumour-associated ECM leads to the enhancement of focal contacts involving integrins and, as a consequence, activation of the PI3 K-Akt pathway, which considerably increases the invasive potential of cancer cells, as has been shown for various tumour entities.[30,92] In this context, lysyl oxidases are apparently not expressed by the neoplastic cells alone, but also by the benign cells of the associated stroma. The gene discussed is AKT1; the disease is neoplasm.