No ontologies were enriched in SS but these tumours showed an upregulation of DNA damage response proteins particularly those involved in non-homologous end joining (NHEJ), including the catalytic subunit of DNA-dependent protein kinase (PRKDC), XRCC1, XRCC5, XRCC6, RAD50 and MRE11 (Fig. S1B and Supplementary Data 3), suggesting that exploiting double-strand break repair mechanisms could be an important therapeutic avenue in this histological subtype27,28. The gene discussed is MRE11; the disease is neoplasm.