RADX is a single-stranded DNA-binding protein that maintains genome stability by regulating RAD51 dynamics at replication forks 1. As an ssDNA binding protein recruited to replication forks, RADX prevents fork collapse by antagonizing RAD51 accumulation to balance fork remodeling and protection 1. Mechanistically, RADX directly interacts with ATP-bound RAD51, stimulates ATP hydrolysis, and destabilizes RAD51 nucleofilaments, thereby inhibiting RAD51 strand exchange and D-loop formation activities 1. This function is independent of RADX's ssDNA binding capability and requires both activities to maintain proper replication fork elongation rates and stability 1. RADX operates in opposition to BRCA2, which can overcome RADX-dependent RAD51 inhibition, ensuring appropriate RAD51 function levels during DNA replication 1. By preventing excessive RAD51 nucleofilament accumulation, RADX avoids genome instability caused by both insufficient and excessive RAD51 activity, thereby protecting cells from replication fork collapse while preserving their capacity to complete homologous recombination of double-strand breaks. This regulatory mechanism is critical for maintaining the delicate balance required for genomic integrity during DNA replication.