However, the facts that silencing each of Bak and Bax modestly but significantly prevented the cytotoxicity of the combination treatment compared with single drugs treatment in HCC cells (Fig 6C and 6D) indicated that FTS pretreatment potentiated the DHA/ARS-triggered Bak/Bax activation and subsequent intrinsic apoptotic pathway, which were further verified by the enhanced effect of FTS on the DHA/ARS-induced ΔΨm loss and cytochrome c release (Fig 3). The gene discussed is BAK1; the disease is hepatocellular carcinoma.