The description of an analogous BIR mechanism underlying ALT in human neoplasia, thought to be initiated by collapsed replication forks (RFs)15,16 was shown to be dependent on RAD52-mediated strand annealing and the yeast pol32 homologue POLD3/49,16 with subsequent studies identifying a RAD52-independent mechanism that was also implicated in ALT-dependent telomere maintenance17,18. The gene discussed is RAD52; the disease is neoplasm.