DNA double strand breaks are among the most detrimental damages which can lead to severe genome rearrangements. The two main repair pathways triggered by DSBs are homologous recombination and nonhomologous end joining repair . It has been proposed that chromatin state and damaged positions determine which pathway is favored [11, 12]. The error-free homologous recombination repair is a multistep procedure containing three main steps: initially (presynaptic phase), DSB is recognized and processed to give a 3’ single-stranded overhang by the MRE11-RAD50-NBS1 (MRN) complex . This 5′–3′ DNA end resection is reinforced by replication protein A (RPA) . Next (synaptic phase), DNA strand invasion takes place when RAD51 binds to single stranded DNA and displaces RPA, which leads to RAD51 polymerization. RAD52 and p53 can control this process . After the homology search, the heteroduplex structure is formed and stabilized by RAD54/p53 complex . Finally (postsynaptic phase), DNA polymerases use the intact sister chromatid strand to re-synthesize fragments and the Holliday junctions are resolved by specific endonucleases that are called as resolvases .