These tumor-promoting functions are achieved via different mechanisms: binding to integrins or CD44 receptor increases the integrin-stimulated FAK-Src-Rho pathway, cancer cell adhesion and survival, while activation of MMPs and matrix remodeling enhances tumor cell invasiveness; PI3K/Akt activation promotes tumor angiogenesis, recruitment of endothelial cells and tumor growth (60, 68). The gene discussed is AKT1; the disease is neoplasm.