Considering that the conserved DREAM complex is highly active in post-mitotic cells and that neurons are particularly susceptible to DNA-repair defects, such as TC-NER defects in Cockayne syndrome, DSB-repair deficiencies in ataxia telangiectasia, or impaired SSB repair in cerebellar ataxia71, targeting of the DREAM complex might provide new therapeutic avenues for a range of congenital DNA-repair deficiencies in humans. The gene discussed is KCNIP3; the disease is Ataxia-telangiectasia.