FBH1 is a 3'–5' DNA helicase that plays a critical role in managing replication stress and maintaining genome stability. As a component of the SCF(FBH1) E3 ubiquitin ligase complex, FBH1 responds to stalled and damaged replication forks by catalyzing fork regression—a process in which the replication fork reverses and nascent DNA strands re-anneal 1. FBH1 prevents excessive homologous recombination by promoting RAD51 filament dissolution from stalled forks, thereby antagonizing recombinogenic activity 2. Additionally, FBH1 acts as the substrate-recognition component of SCF(FBH1), mediating RAD51 ubiquitination to regulate its subcellular localization. Beyond anti-recombinogenic functions, FBH1 promotes cell death in response to severe replication stress; in collaboration with MUS81, it facilitates endonucleolytic DNA cleavage following prolonged replication stress, potentially eliminating cells with excessive genomic damage. FBH1 is recruited to stalled forks through interaction with PCNA 3. Loss of FBH1 results in resistance to replication stress and increased unscheduled recombination, whereas gain of FBH1 has been implicated in a variety of cancers 4. These dual roles—preventing excessive recombination while promoting apoptosis under extreme stress—position FBH1 as a key regulator of the balance between genome protection and cell death.