Given this, individuals that have the heterozygous FUT3 genotype and/or blood group A1 are the most likely to express the non-genuine Lewis-negative phenotype, indicating that the negatively modulating effect of the 59T>G SNP may be accentuated under certain circumstances, either pathological (e.g., inflammations, cancer or metabolic diseases) or physiological conditions, such as pregnancy, which may cause a reduction in the circulatory concentration of active Lewis glycolipids, resulting in the incompatible expression of Lewis antigens in the blood [15], [31]–[32]. Here, FUT3 is linked to metabolic disease.