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Just one decade after its discovery, RNAi technology has not only developed in leaps and bounds but also found its way into human gene therapies and eyed for by biotech companies worldwide in the promise of far-reaching therapeutic applications. This paper is about the progress of research in RNAi in just a few years that led to many current and promising prospects for human therapies based on these cellular mechanisms. Along with its bulk of potential, RNAi-based biotechnology poses a list of questions on how to address problems mostly on aspects of triggered immune responses and safety from side effects when administered exogenously.

History
It was not after 1980 that RNA has been acknowledged as a molecule with an active role in cellular biology. The common notion that RNA was a passive carrier of genetic information from DNA to carry out protein synthesis has been dispelled after the discovery of catalytic RNA. Tom Cech and Sidney Altman both garnered the Nobel Prize for this study. In those days, genes were first defined via description of their mutant phenotype. This was called Forward Genetics, where the phenotype of the resulting mutant gives clues to the function of the gene. At the pace the sequencing of genomes are going now, thousands of genes have been identified yet we only know little of its function. It is therefore more practical, effective and less time-consuming to carry out genetic analysis that proceeds from genotype to phenotype called Reverse Genetics. This can be achieved by a number of gene-manipulation techniques including homologous recombination in embryonic stem cells and antisense approaches.

Ten years ago, Andrew Fire and Craig Mello discovered that (double stranded) dsRNA can trigger silencing of complementary (messenger) mRNA in Caenorhabditis elegans just after its genome sequence was completed in 1998. A new term, RNAi or RNA interference was born. The artificially generated (short interfering) siRNA, which were just short dsRNA, followed soon after that to demonstrate the same mechanism also occurs in mammalian cells, albeit not all the time. The discovery of RNAi related post-transcriptional gene silencing (PTGS) in plants to the activity of dsRNA. They found that the presence of just a few dsRNA molecules was enough to suppress the expression of a gene that was homologous to the dsRNA almost completely.

Many papers followed suit soon after this discovery; and a second wave of studies is currently blossoming as

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