Third, the low posterior probability of shared causal variants in ‘positive control’ co-localisation analyses for GLP1R and BMI could reflect distinct signalling mechanisms influencing type 2 diabetes and BMI in GLP1R, the presence of which would not necessarily influence the validity of this as an instrument for GLP1R signalling perturbation’s effect on glycaemic control [51]. This evidence concerns the gene GLP1R and type 2 diabetes mellitus.