DNA lesions pose a physical obstacle to DNA-dependent cellular transactions such as replication and transcription. A great deal is known regarding RNA polymerase II (RNAP II) transcription stalling in the presence of lesions induced by UV, but recent studies have uncovered previously uncharacterized behavior of the RNAP II machinery in the presence of double strand breaks (DSBs). These new data, although contradictory, contribute to our understanding of a vital cellular mechanism that defends against the production of aberrant transcripts and protects cell viability.