As BRCA2 is involved in localisation of RAD51 and formation of a nucleoprotein filament on DNA at sites of double-strand breaks, we hypothesise that disrupting the interaction between RAD51 filament protomers and between RAD51 and BRCA2 is a valid strategy to increase the susceptibility of tumour cells to radiation and DNA-damaging agents.[22] Therefore, the development of a small molecule that disrupts these interactions by binding at the common FxxA binding site is of interest both as a chemical tool and as a potential therapeutic compound. This evidence concerns the gene BRCA2 and neoplasm.