The chief strengths of the present study include the large number of proteins assayed, independent replication of the main results internally and externally, use of ancestry-specific genetic instruments to assess causality, exclusion of CKB data from AGEN T2D GWAS summary statistics to minimize potential collider bias resulting from sample overlap, and multiple downstream analyses to assess possible mechanisms underlying these associations. Here, CKB is linked to type 2 diabetes mellitus.