This term differentiates the isolated MSH3 dysfunction observed in inflammation-associated microsatellite alterations from secondary MSH3 mutations as a result of MLH1 deficiency in sporadic CRCs, a scenario where a tumor would manifest mononucleotide frameshifts in addition to di-, tri-, and tetranucleotide instability (9,16,17). This evidence concerns the gene MSH3 and neoplasm.