ZNF830 is a zinc finger protein that functions as a critical regulator of DNA homologous recombination (HR) repair and cell cycle progression. Mechanistically, ZNF830 promotes HR repair by directly interacting with CtIP and facilitating DNA end resection at double-strand break sites 1. The protein binds preferentially to double-stranded DNA with 3' or 5' overhangs through its zinc finger domain, with recruitment to DNA damage sites dependent on ATR-mediated phosphorylation at serine 362 1. ZNF830 also interacts with the ubiquitin E3 ligase PPIL2, which regulates CtIP ubiquitination and modulates HR efficiency 2. Beyond DNA repair, ZNF830 participates in pre-mRNA splicing as a spliceosome component and controls mitotic progression while preventing replication fork collapse and double-strand break formation in rapidly proliferating cells. Clinically, ZNF830 overexpression confers chemoresistance to genotoxic therapy in cancer cells 1, and genetic variants in ZNF830 are associated with variable radiation therapy-induced adverse skin reactions in breast cancer patients, acting as a genetic modifier of normal tissue toxicity 3. These findings establish ZNF830 as a multifunctional protein linking genome maintenance to cancer treatment resistance.