PCNA (proliferating cell nuclear antigen) is a homotrimeric ring-shaped processivity factor essential for DNA replication and repair 1. It encircles DNA and slides along it, tethering DNA polymerases delta and epsilon to increase their processivity during leading strand synthesis 1. PCNA serves as a dynamic molecular hub that coordinates replication with DNA damage response by recruiting repair proteins through PCNA-interacting protein box (PIP-box) motifs 1. Following replication fork stalling, monoubiquitination of PCNA at lysine 164 recruits translesion synthesis polymerases (REV1, POLζ) for error-prone lesion bypass 2. Alternatively, K63-linked polyubiquitination engages error-free homologous recombination pathways 3. PCNA K164 ubiquitination also promotes FANCD2-dependent mitotic DNA synthesis to resolve under-replicated regions 3. After fork restart, ATAD5-containing complexes actively de-ubiquitinate PCNA to restore replication fidelity 4, with BAZ1B modulating timely de-ubiquitination to prevent premature resumption 5. Dysregulation of PCNA cycling impairs genome stability; checkpoint failure causes PCNA/RFC sequestration by excess DNA synthesis, triggering HLTF-mediated fork collapse 6. These mechanisms underscore PCNA's critical role in coordinating replication fork progression with DNA damage tolerance.