RAD51B is a critical component of the homologous recombination (HR) DNA repair pathway, functioning within the RAD51B-RAD51C-RAD51D-XRCC2 (BCDX2) tumor suppressor complex 1. Structural analyses reveal that RAD51B exhibits high dynamics within this tetrameric complex, where it works alongside other RAD51 paralogs to orchestrate RAD51 filament assembly on single-stranded DNA for replication fork protection and double-strand break repair 1. The BCDX2 complex stimulates both nucleation and extension of RAD51 filaments through coupled ATPase activities of RAD51B and RAD51C, which are essential for recombinational DNA repair 1. RAD51B dysfunction contributes significantly to cancer predisposition, with germline mutations found in ovarian cancer patients at frequencies of 0.06% and associated with increased cancer risk 2. The gene also shows somatic alterations in various cancers - whole-genome sequencing identified RAD51B breakage as a common mechanism for tumor suppressor inactivation in high-grade serous ovarian cancer 3, and noncoding regulatory mutations near RAD51B have been identified as possible cancer drivers 4. These findings establish RAD51B as both a guardian of genome stability and an important cancer susceptibility gene whose loss of function promotes tumorigenesis.