The normal DNA repair machinery is essential for maintaining genome stability, yet it has a dark side: it makes mistakes at repetitive sequences. The resulting rearrangements can be evolutionary beneficial or cause pathologies. For instance, the expansion of CAG/CTG repeats causes at least 14 different neurological disorders that all remain without a cure. Since the longer the CAG/CTG tract, the more severe the symptoms are, it has been proposed that contracting the repeat tract to a normal length may provide a therapeutic avenue. Expansions, by contrast, would exacerbate the disease. Here I will talk about two different projects: 1) how the CRISPR-Cas9 nickase can be used to contract expanded repeat tract specifically. 2) How we can use a novel inducible chromatin targeting assay to dissect the local role of chromatin structure in expanded repeat instability and expression.