Living organisms are in threats of endogenous/exogenous DNA damages. DNA damage impedes both replication and transcription accuracy. To ensure correct replication and transcriptions, and subsequent genome integrity and genetic stability, living organisms have evolved different mechanisms for DNA repair. This review focused on RNA polymerase surveilled (RNAP-S) mechanisms for DNA repairs, and discussed biological significance of the RNAP-S repairs and perspectives. RNA polymerase (RNAP) structure is a complex, being composed of many subunits with different roles in RNAP function. RNAPII has a trigger loop (TL) and a bridge helix (BH), these domains sense DNA lesions during transcription. RNAP stalls at the DNA damage sites to avoid transcribing mutated mRNA, allowing the repair system to be recruited. Interestingly, Mfd and DksA dissociate the stalled RNAP while UvrD pulls back the stalled RNAP on the template DNA to expose the lesions for subsequent performance of lesion repairs. Similarly, the CSB protein, its ubiquitination and OGG1 mediate RNAP-S repairs in eukaryotic cells. Most recently, it has been shown that RNAPIII is involved in homologous recombination repair.