So, due to increased interest in developing new ways of targeting RAD52 activity and expression, Huang et al. identified seventy potential inhibitor molecules capable of altering RAD52 function and consequently inhibiting the ssDNA annealing capacity of RAD52. In practical context, it was possible to observe that in hereditary ovarian and breast cancers with a defective activity of BRCA1/2 genes and inactivation of RAD52 function, by specific inhibitors, there was an induced suppression of tumor cells progression (Figure 3) [69]. The gene discussed is RAD52; the disease is breast cancer.