The phenomenon of double-stranded RNAs (dsRNAs)-mediated gene silencing or RNA interference (RNAi] was first discovered in nematode Caenorhabditis elegans by Andrew Fire and Craig Mello in 1998 [1]. This great discovery gives rise to a fast-growing field and leads to the identification of novel RNAi pathways by which small interference RNAs (siRNAs) regulate gene expression and gene functions. Collective evidence suggests that the RNAi pathway is conserved in many eukaryotes and this pathway can be triggered by either exogenous or endogenous small interference RNAs. Exogenous dsRNAs (e.g. a virus with an RNA genome) are typically required a membrane transporter for dsRNA uptake into the cytoplasm, while endogenous small interference RNAs (e.g. microRNAs) are encoded in the genome. The precursors of both dsRNA and microRNA are first cleaved into short interference RNAs by a ribonuclease III (RNaseIII) enzyme, Dicer. Then these short

interference RNAs initiate RNAi process when interacting argonaute proteins in the RNAinduced silencing complex (RISC). The small interference RNAs normally consist of 20~30 nucleotides. They can repress the transcription of message RNAs containing homologous sequences by either post-transcriptional gene silencing (PTGS) or transcriptional gene silencing (TGS) [2].