The additional depletion of CSB (Cockayne Syndrome B), a TC-NER factor, further reduced UDS in ASH1L–/– cells (Fig. 1h; see Supplementary Fig. 3 for the efficiency of siRNA-mediated depletions), thus establishing that ASH1L is required for GG-NER activity in response to CPDs in the same manner as XPC, and that the remaining excision in ASH1L–/– cells is mostly due to the TC-NER pathway. Here, ASH1L is linked to Cockayne syndrome.