MMS22L encodes a DNA repair protein that functions as part of the MMS22L-TONSL heterodimer complex, which plays a central role in protecting genome integrity during DNA replication. The complex promotes homologous recombination-mediated repair of double-strand breaks at stalled or collapsed replication forks by mediating RAD51 filament assembly on single-stranded DNA; MMS22L directly binds ssDNA and interacts with RAD51 to facilitate strand exchange activity 1. The complex recognizes post-replicative chr6 through the TONSL subunit's binding to unmethylated histone H4K20 marks specific to newly synthesized histones, enabling targeted recruitment to replicated DNA and DNA lesions 2. MMS22L also functions in sister chr6 cohesion establishment through a pathway parallel to DSCC1-RFC 3. Clinically, MMS22L deletions occur in up to 14% of prostate cancers and render cells hypersensitive to PARP inhibitors by impairing RAD51 loading—a TP53-dependent effect that could inform therapeutic biomarker selection beyond BRCA1/2-deficient tumors 4. In erythropoiesis, loss of MMS22L causes proliferation and differentiation arrest with p53 pathway activation, and combined mms22l and cdan1 haploinsufficiency results in severe anemia in zebrafish models, indicating MMS22L's indispensable role in normal blood cell development 5. Pan-cancer analysis reveals MMS22L as a tumor-regulating gene with prognostic implications, particularly in hepatocellular carcinoma 6.