Haugen et al. experimentally linked the first connection between EMAST and MSH3 in human colon cancer, showing: (a) loss of expression of MSH3 in colorectal cancers with EMAST; and (b) that MSH3-deficient cells (deficient background or through knockdown of MSH3) exhibited dinucleotide or greater microsatellite frameshift mutation [16]. The gene discussed is MSH3; the disease is colorectal cancer.