Unlike yeast RAD52, although human RAD52 is considered to lack mediator activity, IR-induced RAD52-RAD51 lesions can readily form in the presence or absence of BRCA2.15,16 Accumulating evidence has shown the crucial role and complex mechanisms of human RAD52 with RAD51 in HR through BRCA2-independent mechanisms, including RAD51 recruitment to active DSBs sites, filament stabilization, and multiple invasions.16,47–50 The functions of RAD52 were recapitulated in our IR-induced models, underscoring the indispensable role of RAD52 in RAD51-dependent HR of HCC. This evidence concerns the gene RAD51 and hepatocellular carcinoma.