an increase in copy number of a particular region of the genome. During the repair of a double stranded break, the broken end can invade its homologous chromosome instead of rejoining the original strand. As in the non-allelic homologous recombination mechanism, an extra copy of a particular region is transferred to another chromosome, leading to a duplication event. Furthermore, cohesin proteins are found to aid in the repair system of double stranded breaks through clamping the two ends in close proximity which prevents interchromosomal invasion of the ends. If for any reason, such as activation of ribosomal RNA, cohesin activity is affected then there may be local increase in double stranded break repair errors. The other class of possible mechanisms that are hypothesized to lead to copy number variations is non-homologous based. To distinguish between this and homologous based mechanisms, one must understand the concept of homology. Homologous pairing of chromosomes involved using DNA strands that are highly similar to each other (~97%) and these strands must be longer than a certain length to avoid short but highly similar pairings. Non-homologous pairings, on the other hand, rely on only few base pairs of similarity between two strands, therefore it is possible for genetic materials to be exchanged or duplicated in the process of non-homologous based double stranded repairs. One type of non-homologous based mechanism is the non-homologous end joining or micro-homology end joining mechanism. These mechanisms are also involved in repairing double stranded breaks but require no homology or limited micro-homology. When these strands are repaired, oftentimes there are small deletions or insertions added into the repaired strand. It is possible that retrotransposons are inserted into the genome through this repair system. If retrotransposons are inserted into a non-allelic position on the chromosome, meiotic recombination can drive the insertion to be recombined into the same strand as an already existing copy of the same region. Another mechanism is the break-fusion-bridge cycle which involves sister chromatids that have both lost its telomeric region due to double stranded breaks. It is proposed that these sister chromatids will fuse together to form one dicentric chromosome, and then segregate into two different nuclei. Because pulling the dicentric chromosome apart causes a double stranded break, the end regions can fuse to other double stranded breaks and repeat the cycle. The fusion of two sister chromatids can cause inverted duplication and when these events are repeated