ATAD5 is a critical DNA replication and genome stability factor that functions as the major subunit of a replication factor C-like complex (RFC-like complex) 1. Its primary function is to unload the ring-shaped PCNA homotrimer from DNA following replication in an ATPase-dependent manner 2, preventing abnormal PCNA accumulation on chr17 3. ATAD5 functions as a regulatory scaffold for PCNA deubiquitination, recruiting the UAF1-USP1 deubiquitinase complex and enhancing deubiquitination by USP7 and USP11 to facilitate resumption of high-fidelity DNA synthesis after lesion bypass 4. This process is fine-tuned by BAZ1B interaction, which prevents premature deubiquitination and protects genomic integrity 5. During replication stress, ATAD5 promotes replication fork restart by recruiting RAD51 in an ATR-dependent manner while removing PCNA as a mechanical barrier to fork regression 6. Additionally, ATAD5 localizes to centrosomes where it suppresses over-duplication through UAF1-mediated regulation 7. ATAD5 deficiency causes genomic instability and tumorigenesis 1, and rare missense variants are enriched in ovarian cancer patients 8. ATAD5 also modulates DNA repeat instability across tissue types 9.