Down-regulated expression of AP-4, p21 and p53 in the meanwhile could make the cell cycle arrest caused knockdown of AP-4 disappearance. These results are in agreement with a model in which AP-4 induces cell cycle arrest by regulating the expression of cell cycle regulators, such as p53, p21 and cyclin D1. Apoptosis, or programmed cell death, is known to participate in various biological processes by two main apoptotic pathways, the mitochondrial pathway and the death receptor pathway. We found that silencing the AP-4 expression trigged cell apoptosis in our experiment, which demonstrated that AP-4 suppressed apoptosis in human gastric Oligomycin A ATPase inhibitor cancer cells. In our experiment, increasing levels of Caspase-9 and downregulation of Bcl-2 and Bcl-xL were detected in human gastric cancer cells, indicating that knockdown of AP-4 activated both intrinsic and extrinsic pathways to apoptosis in cancer cells. In summary, the data demonstrate that RNAi-mediated downregulation of transcription factor AP-4 effectively inhibited the cell proliferation, indicated cell cycle arrest, triggered apoptosis and enhanced chemo-sensitivity of human gastric cancer cells with the decreased expression of cyclin D1, Bcl-2 and Bcl-xL and activated p21, p53 and Caspase-9 expression, which suggested AP-4 may be a oncogene playing an important role in tumorigenesis. Although the precise mechanism of this role needs to be further investigated, the AP-4specific-siRNAs may be of potential values as novel therapeutic agents for human gastric cancer. Most Hepatitis C virus infections evolve in persistent infection, which may progress to fibrosis, cirrhosis, liver failure or even hepatocellular carcinoma. Current standard therapy is based on a combination of pegylated -IFN-a and ribavirin and treatment response may be influenced by several virusrelated factors such as HCV genotype and baseline titer of HCV RNA. A sustained virological response occurs in approximately 80% of patients infected with HCV genotypes 2 or 3, and in approximately 45% for genotypes 1 or 4. New antiviral strategies are currently in development for HCV infection and include drugs targeting key viral enzymes such as NS3-4A and the NS5B RNA-dependent RNA polymerase. Although effective, the use of these new antivirals seems associated to the selection of drug-resistant HCV variants, resulting in viral breakthrough. Thus, a combination between antivirals and standard treatment with IFNa and RBV is therefore necessary. HCV persistence is mainly due to the failure of the host’s immune system to effectively and definitively clear the infection and generate protective cellular immunity. Indeed, marked quantitative and qualitative defects of HCV-specific CD8 T-cells have been described in HCV patients, correlated with innate immune cell impairment such as dendritic cell and NK cells. In this context, immune modulation could represent a promising strategy aimed to restore protective immune response, inducing a long lasting immunity, necessary to obtain viral eradication. Among innate immune cells, Vc9Vd2 T-cells represent a good target for immunotherapy in infectious diseases for their multifaceted response capability. They may specifically be activated both in vitro and in vivo by using phosphoantigens and aminobisphosphonates without any MHC restriction.