In general, colorectal tumours arising secondary to pathogenic MUTYH, POLE, POLD1, and NTHL1 germline variants are microsatellite-stable (MSS), and involve somatic variants in driver genes of classical colon tumourigenesis pathways, such as APC, KRAS, PIK3CA, FBXW7, or TP53. This evidence concerns the gene APC and colorectal neoplasm.