Other studies [44, 45] have shown that less than 0.1 % of CRC have inherited mutations at characteristic sites within the exonuclease domain of either POLE (p.Leu424Val) or POLD1 (p.Ser478Asn), which are the basis of the polymerase-proofreading-associated polyposis (PPAP) syndrome that is characterised by increased colorectal adenomas and adenocarcinomas as well as increased risk of endometrial cancer in the case of inherited POLD1 mutations [44]. The gene discussed is POLE; the disease is colorectal carcinoma.