ARID4B and type 2 diabetes mellitus: Our findings support a causal role of BCAA because 1) both CVD and T2D risk variants were enriched in the co-expression modules related to BCAA degradation, and 2) 15 genes in the BCAA pathway were part of the top KD subnetworks, representing a significant enrichment of BCAA genes (fold enrichment = 3.02, Fisher’s exact test p = 1.4e-5).