Additionally, we evaluated 158 clinically unselected GCK variant carriers from the UK Biobank to examine polygenic effects independent of clinical referral.<h4>Results</h4>We observed independent polygenic enrichment for HbA<sub>1c</sub> (including both glycaemic and non-glycaemic components), fasting glucose and type 2 diabetes in clinically referred GCK-MODY individuals compared with non-diabetes controls (0.16-0.33 SD higher, all p<0.003), but not for type 1 diabetes. The gene discussed is GCK; the disease is diabetes mellitus.