In the past few months, several discoveries relating to the mechanism underlying transcription-coupled DNA repair (TCR) have been reported. These results make it timely to propose a hypothesis for how eukaryotic cells might deal with arrested RNA polymerase II (Pol II) complexes. In this model, the transcription-repair coupling factor Cockayne Syndrome B (or the yeast equivalent Rad26) uses DNA translocase activity to remodel the Pol II-DNA interface, possibly to push the polymerase past the obstruction or to remove it from the DNA so that repair can take place if the obstacle is a DNA lesion. However, when this action is not possible and Pol II is left irreversibly trapped on DNA, the polymerase is instead ubiquitylated and eventually removed by proteolysis.