Therefore, chemical inhibition of RAD51-BRCA2 interaction to mimic the BRCA2 mutation phenotype (i.e. BRCAness) presents a compelling avenue for intervention, as it could be applied in a fully small molecule-induced synthetic lethality anticancer strategy for difficult-to-treat tumours, including PARPi-resistant and BRCA-proficient pancreatic ductal adenocarcinoma (PDAC). Here, RAD51 is linked to neoplasm.