Consistently, expression of a MMR-deficient MSH2 missense mutation (MSH2-A834T) found in hereditary non-polyposis colorectal cancer families (43) is able to rescue REV1 focus formation in MSH2-depleted cells (Supplementary Figure S7), suggesting that the role of MSH2 in MMR and TLS could be separable, which might be useful in the development of novel strategies to reduce unwanted mutagenesis that promotes tumor resistance. The gene discussed is MSH2; the disease is neoplasm.