Since magnesium is an essential cofactor in major enzymatic systems involved in DNA replication and repair16, and is an absolute requirement for downstream execution of BER pathways17, chronic magnesium deficiency due to Gitelman syndrome could possibly further abrogate BER efficiency in the setting of MUTYH deficiency, increasing susceptibility to oxidative stress and enabling the phenotypic manifestation of monoallelic MUTYH mutation in this patient. This evidence concerns the gene MUTYH and Gitelman syndrome.