also associated with “pathological” FG levels and T2D risk. Thus, variation in FG in healthy individuals is not necessarily an endophenotype for T2D, which posits the hypothesis that the mechanism by which glucose is raised, rather than a mere elevation in fasting glucose levels, is a key contributor to disease progression. On the other hand, we cannot rule out the existence of protective variants in loci where elevated FG does not progress to manifest T2D, or the effect of cohort selection in the detection of the loci with variable effects on FG and T2D risk. Nevertheless, this work shows that targeting quantitative traits in GWAS searches can help identify genetic determinants of overt disease.
