CRISPR-Cas systems confer bacteria and archaea an adaptive immunity against phages and other invading mobile genetic elements. In type II CRISPR-Cas systems, the Cas9 protein introduces double strand breaks in target DNA. The outcome of a break introduced by Cas9 will determine whether the target molecule is destroyed, repaired, or a mutation is introduced. This will depend on the DNA repair pathways present in the cell as well as the availability of a template molecule for repair through homologous recombination. Deciphering the consequences of Cas9 breaks is critical both in the development of novel genetic engineer tools and to better understand the selective pressures controlling CRISPR evolution in relationship with DNA repair pathways. Here I will first detail the consequences of Cas9 breaks in the chromosome of E. coli. I will then present a comparative genomic analysis on the interplay between DNA repair pathway and CRISPR systems. We report a negative association between NHEJ and Type IIA CRISPR Cas systems which was further investigated experimentally.  Our findings provide insights into the complex interactions between CRISPR-Cas systems and repair mechanisms in bacteria.