Further, a minority of tumours (<10%) exhibit hypermutator phenotypes, for instance in tumours associated with defective base excision repair (e.g., MUTYH inactivation), mismatch repair (e.g., MSH2, PMS2, MLH1 inactivation) or APOBEC cytidine deaminase activity mutational signatures [8,9,12,14,17,18,19]. This evidence concerns the gene MSH2 and neoplasm.