These findings are in line with mice studies: Compared to Apc1638N mice deficient for MSH6, which predominantly showed somatic base-pair substitutions of the wild type APC allele (just 5 of 76 variants were indels), most of the APC variants in MSH3-deficient Apc1638N mice (5/7) were frameshift variants, and of these, three were dinucleotide insertion/deletions that were not found in other MMR-deficient Apc1638N tumours, and two were large (≥8 bp) deletions [46]. The gene discussed is MSH6; the disease is neoplasm.