MLH1 and carcinoma: Mice that were deficient in DNA mismatch repair (MMR) due to homozygosity for a null allele of Mlh1 develop normally but are prone to lymphomas, intestinal adenomas and carcinomas, and skin gland tumors [14], on the other hand antioxidant-related nutrients can enhance DNA repair activity by modifying gene expression distinct from their direct antioxidant properties and are protective for lymphoma [15].