This accounts for about 15% of CRCs, including patients with the hereditary cancer syndrome of Lynch syndrome, and carries distinct features compared to other tumour types.136–138 Approximately 80% of cases of sporadic mismatch-repair deficiency (dMMR) in CRC are due to MLH1 gene promoter methylation, and over 70% of hereditary dMMR incidents are coupled with MLH1 and MSH2 germline mutations.138–140 Only approximately 4% of mCRCs are deemed as dMMR tumours, whereby upwards of 30% of the microsatellite marker panel are mutated. Here, MSH2 is linked to neoplasm.