This either suggests that RAD51C may not be essential for ALT or that, unlike the model, ALT-mediated telomere synthesis in neuroblastoma favors the RAD51-associated and RAD52-independent pathway, further supported by high prevalence of C-circles in ALT neuroblastomas,31 as well as the prognostic value of and chemotherapy resistance conferred by RAD51 expression in this disease.88 The gene discussed is RAD51C; the disease is neuroblastoma.