['Skin fluorescence (SF) is a non-invasive marker of AGEs and is associated with the long-term complications of diabetes. SF increases with age and is also greater among individuals with diabetes. A familial correlation of SF suggests that genetics may play a role. We therefore performed parallel genome-wide association studies of SF in two cohorts.', 'Cohort 1 included 1,082 participants, 35-67\xa0years of age with type 1 diabetes. Cohort 2 included 8,721 participants without diabetes, aged 18-90\xa0years.', 'rs1495741 was significantly associated with SF in Cohort 1 (p\u2009<\u20096\u2009×\u200910(-10)), which is known to tag the NAT2 acetylator phenotype. The fast acetylator genotype was associated with lower SF, explaining up to 15% of the variance. In Cohort 2, the top signal associated with SF (p\u2009=\u20098.3\u2009×\u200910(-42)) was rs4921914, also in NAT2, 440 bases upstream of rs1495741 (linkage disequilibrium r (2)\u2009=\u20091.0 for rs4921914 with rs1495741). We replicated these results in two additional cohorts, one with and one without type 1 diabetes. Finally, to understand which compounds are contributing to the NAT2-SF signal, we examined 11 compounds assayed from skin biopsies (n\u2009=\u2009198): the fast acetylator genotype was associated with lower levels of the AGEs hydroimidazolones of glyoxal (p\u2009=\u20090.017).'] Does gWAS identify an NAT2 acetylator status tag single nucleotide polymorphism to be a major locus for skin fluorescence?