EDITORGenetic factors are clearly implicated in colorectal cancer (CRC) susceptibility, with 10% of all cases having an affected first degree relative and suggestions that up to 20% of all colorectal cancers occur in susceptible people. Identification of the molecular basis for familial adenomatous polyposis (FAP) and hereditary non-polyposis colon cancer syndrome (HNPCC) has provided insights into the mechanisms of colorectal cancer susceptibility and illustrated how somatic mutations in familial cancer genes are frequently implicated in sporadic cancers. FAP has a characteristic phenotype with profuse colorectal polyposis, and although variant attenuated forms of FAP are described, germline APC gene mutations are a rare cause of colorectal cancer. HNPCC is characterised by early onset CRC and, in some kindreds, endometrial, gastric, ovarian, pancreatic, and urinary tract cancers.¹ Germline mutations in mismatch repair genes (MMR) such as MSH2, MLH1, PMS1, PMS2, and MSH6 account for many, but . . . [Full text of this article]