Scientists discovered that a well-known DNA repair pathway, the Fanconi anemia pathway, surprisingly plays a key role in repairing double-strand DNA breaks created by CRISPR-Cas9. It acts as a traffic cop to steer repair to simple end-joining or to patching the cut with new, single-strand DNA. Scientists could potentially tweak proteins involved in the pathway to preferentially steer the outcome toward replacement with DNA, which is important for gene therapy for hereditary diseases.