RAD54B is a multifunctional ATPase that plays a redundant role with RAD54 in homologous recombination (HR), the major pathway for repairing DNA double-strand breaks (DSBs) 1. As a molecular motor, RAD54B facilitates homology search by guiding RAD51 along donor DNA, converting diffusion-based mechanisms to motor-guided processes 1. Unlike its structural homolog RAD54, RAD54B exhibits lower ATP hydrolysis rates and does not directly interact with RAD51 1. RAD54B also functions as a molecular adapter promoting MDM2-MDM4 heterodimerization to facilitate p53 degradation, thereby modulating cellular responses to DNA damage 2. Clinically, RAD54B has paradoxical roles in cancer. RAD54B is frequently upregulated in gastric cancer, promoting cell migration and angiogenesis via the Wnt/β-catenin pathway 3. In bladder cancer, elevated RAD54B expression confers chemotherapy resistance by enhancing DNA repair when stabilized by the AP1M2/PUM1 pathway 4. Conversely, RAD54B mutations in ovarian cancer impair HR repair, increasing DNA damage and sensitizing cells to PARP inhibitors, suggesting therapeutic potential 5. The INO80 chr8-remodeling complex regulates RAD54B expression to facilitate DSB repair 6. These findings position RAD54B as both an oncogenic driver and potential therapeutic target depending on cancer context.