The role of somatic MYH mutations in CRC seems to be confined to cases with moderate adenoma counts (10–1000), rather than extensive polyposis (>1000 adenomas).143 In situations where an APC mutation is absent, MYH somatic mutations may account for approximately 8–20% of polyposis cases.144 It has been suggested that the cancer phenotype associated with MYH mutations may be as prevalent as FAP. This evidence concerns the gene FAP and polyposis.