As obtained in studies of non-malignant breast cells or patient-derived organ tissues, MGO induces cancer-associated mutant single base substitutions (SBS), triggers BRCA2 proteolysis, and transiently disables the tumor-suppressor function of BRCA2 in DNA repair and replication, leading to functional haploinsufficiency (35, 36). This evidence concerns the gene BRCA2 and neoplasm.