An important mechanism required for genome stability is the protection of stressed replication forks by fork reversal and nascent strand protection, a process mediated by the concerted action of the RAD51 recombinase and the BRCA1-BRCA2 tumour suppressor pathway, in addition to a series of fork remodellers and processing enzymes (Quinet et al, 2017). This evidence concerns the gene BRCA1 and neoplasm.