We found that sorafenib-induced attenuation of anti-apoptotic Bcl2 and Bcl-xL and induction of apoptotic cleaved caspase-3 were inhibited in the presence of HGF in control cells; however, following knock-down of Nrf2, the HGF treatment could not either increase Bcl2/Bcl-xL or decrease caspase-3 in sorafenib-treated cancer cells as compared with controls (Fig. 2e). The gene discussed is BCL2; the disease is cancer.