MRC1 and neoplasm: The majority of these studies contained patients with somatic hypermethylation of the hMLH1 promoter, rendering the tumor completely MMR-deficient because for repair to occur after DNA synthesis, both recognition of mismatch in the DNA by either hMutSα or hMutSß and signaling for excision of the mismatch by a second heterodimer, hMutLα (consisting of the MMR proteins hMLH1 and hPMS2), are essential.