On the contrary, other members of the family, dependent on Rac1 and activated by TGF-β, might have opposite effects [59], such as inhibition of the epidermal growth factor (EGF) pathway, which enhances TGF-β induced apoptosis in rat hepatoma cells, thus inducing oxidative stress via increased ROS production, coincident with a change in the expression pattern of the NOX isoforms [66,67]. The gene discussed is TGFB1; the disease is hepatocellular carcinoma.