T2D-PRS contributed to the onset of (any) diabetes among the participants: in a Cox proportional hazards model, 1 SD unit increase in T2D-PRS increased the risk of diabetes by 28% (HR 1.28; 95% CI 1.065, 1.535; p=0.00841; with the HNF1A carrier status as a significant covariate: HR 22.1, p<2 × 10−16). This evidence concerns the gene HNF1A and diabetes mellitus.