The expansion propensity and mutation rate results suggest a tradeoff in which too little Msh3 may result in an MMR deficiency (as seen in EMAST) (Campregher et al. 2012), whereas increased Msh3 activity results in more MMR activity but biases mutations toward expansions (as previously observed at the Huntington's disease and other repeats (Fig. 5; Wheeler and Dion 2021). This evidence concerns the gene MSH3 and mismatch repair cancer syndrome 1.