Synopsis: “DNA double-strand breaks (DSBs) are highly toxic and their accurate repair is essential for the prevention of human disease and cancer. However, in developing B and T lymphocytes, mutagenic DSB repair is instead favoured and mediates genetic recombination within antibody/B cell and T cell receptor genes, the result of which creates diversity in immune repertoire. To cope with this intrinsic discrepancy in desired DNA repair outcome between different contexts and tissue types, cells have evolved complex regulatory systems that maintain an appropriate equilibrium between competing DNA repair pathways, and that ensure DNA breaks are appropriately resolved. This talk will focus on my groups’ recent research into the molecular mechanisms that underpin a cell’s ability to select between accurate and mutagenic DNA repair pathways, and will describe how understanding these processes can inform on the molecular basis of cancer and its response to therapy