Our lab focuses on understanding how cells maintain the stability of their genome in the context of 3D genome organization. We are interested in shedding light on when, where and why chromosomes become fragile, how this mechanistically occurs, and how DNA repair mechanisms prevent the illegitimate joining that leads to the formation of oncogenic genome rearrangements. Our work is focused on intrinsic or exogenous sources of DNA fragility and on DSBs that form upon the use of CRISPR/Cas genome editing nucleases.