In recent years, RNA interference (RNAi) has gained a lot of interest as a tool for functional genomics studies and probably equally important as a promising therapeutic approach for the treatment of various diseases [72, 73] . RNAi is a highly evolutionally conserved and specific process of post-transcriptional gene silencing (PTGS) by which double stranded RNA (dsRNA), when introduced into a cell, causes sequence-specific degradation of homologous mRNA sequences [74, 75] . Mechanistically the process can be divided into two steps. An initiator step where dsRNA is cleaved by dicer, a member of the RNase III family, into 21-25 nt long small interfering RNA (siRNA) fragments [76] . In a consecutive step, these fragments are transferred to RISC (RNAinduced silencing complex) where one of the strands, the so called guide strand, serves as a molecular template to recognize homologous mRNA that is cleaved by Argonaute [77, 78] , a protein component of RISC. Once the guide strand is bound to RISC this complex can undergo many rounds of mRNA binding and cleavage ( [79] , Fig. (3A) ). To circumvent application of long double stranded RNAs, which inevitably trigger an interferon response, it is sufficient to extracellularly supply 21 nt long dsRNAs [80, 81] . Alternatively, siRNAs can be expressed endogenously using DNA vectors which code for short hairpin (sh) RNAs [82] [83] [84] . These shRNAs are than cleaved by dicer to siRNAs. Short hairpin RNA constructs have advantages over siRNA because the effects of these constructs can lead to a more stable and long-term result. On the other hand, besides the fact that shRNAs might interfere with the microRNA pathway [85, 86] , this strategy requires a gene therapy approach in the long run [87] . For this reason we will not cover shRNAs.