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Abstract
Nearly 9 years ago, Fire and Mello and their colleagues reported that exposing cells of the nematodt- Caenorhabditis elegans to double-stranded RNA resulted in specific and efficient gene silencing.1 They also observed that double-stranded UNA is far more potent than sense or antisense RNA in silencing the gene that shares its sequence, and they dubbed the silencing process "RNA interference" (RNAi). Nevertheless, the successful application of RNAi to a broad range of animal models of disease - for diseases such as amyotrophic lateral sclerosis, spinocerebellar ataxia, and atherosclerosis and infections caused by the respiratory syncytial virus, parainfluenza virus, herpes simplex virus 2, and the hepatitis B and C viruses - augurs well.