Fine-mapping identified a credible set of causal variants including non-coding variants and missense coding variants in SLC16A11. Liver expression data and chromatin modification analysis showed reduced SLC16A11 expression and less-activating histone modifications in samples from T2D risk allele carriers, thus proposing SLC16A11 as the candidate causal gene. The gene discussed is SLC16A11; the disease is type 2 diabetes mellitus.