Rnaseh2b, a subunit of the RNase H2 endonuclease complex, plays a crucial role in ribonucleotide excision repair by cleaving RNA in RNA:DNA hybrids [2,5]. This function is essential for maintaining genomic stability, and its associated pathways are vital for normal cellular function. Genetic models, such as KO or CKO mouse models, are valuable tools for studying Rnaseh2b's function.

Mutations in Rnaseh2b are associated with Aicardi-Goutières syndrome, an inflammatory disorder [2,3,4,5,7]. In patients with this syndrome, there is an increase in type I interferon activity, and a subset of patients with Rnaseh2b mutations may have a less severe phenotype and lower mortality compared to those with mutations in other related genes [2,5]. In prostate cancer, loss of Rnaseh2b can sensitize tumor cells to PARP inhibition, but co-deletion of adjacent RB1 can override this sensitivity [1,6].

In conclusion, Rnaseh2b is essential for ribonucleotide excision repair and maintaining genomic stability. Studies using genetic models have revealed its role in diseases like Aicardi-Goutières syndrome and prostate cancer. Understanding Rnaseh2b's function provides insights into disease mechanisms and potential therapeutic strategies for these conditions.