We next found that deficiencies in genes in other DSB repair pathways, that is, HR (brc-1, the worm homologue of mammalian breast cancer gene BRCA1) or single-stranded annealing (xpf-1/ercc-1) also did not affect the mutation spectrum of insertions/deletions (indels) at Tc1-induced breaks (Fig. 1c and Supplementary Fig. 2), nor did defects in mismatch repair or translesion synthesis (Supplementary Fig. 2 and Supplementary Data 4). The gene discussed is BRCA1; the disease is breast carcinoma.