Previous authors have speculated that interactions between folate and MTHFR polymorphism may be elicited to show that (a) the lower activity of variant genotypes may increase the risk of breast cancer at low levels of dietary folate since less 5-methyl THF is made available for DNA methylation, and (b) variant genotypes might provide advantages over the wild genotype in folate-replete conditions since 5,10-methyl THF would be available for nucleotide synthesis [2,4]. This evidence concerns the gene MTHFR and breast carcinoma.