RAD52 and Fanconi anemia: Previous studies have shown that genome editing using dsDNA donors relies on canonical RAD51-mediated HDR, also known as homologous recombination, while ssODN-mediated genome editing depends on single-stranded template repair (SSTR), a RAD51-independent HDR process that is promoted by RAD52 and proteins of the Fanconi anemia pathway4,24,33–36.