Genetic risk of type 1 diabetes (T1D) is primarily non-coding, and single cell epigenomics enables dissecting non-coding risk variant function at cell type resolution. In a recent study, we combined genetic association mapping of T1D risk with cis-regulatory programs in pancreas and peripheral blood cell types defined using snATAC-seq. T1D-associated variants were enriched in candidate cis-regulatory elements (cCREs) in T cells and beta cells, as well as unexpectedly in pancreatic acinar and ductal (exocrine) cells. Variants at multiple T1D loci mapped in exocrine-specific cCREs linked to genes with exocrine-specific expression, including T1D variants in a ductal-specific cCRE that regulated CFTR expression. Next, in on-going studies, we are performing expanded profiling of cis-regulatory programs in pancreas cell types using snATAC-seq and snRNA-seq in 34 control, T1D autoantibody positive, and T1D samples. Preliminary analyses revealed marked changes in beta cell cCRE activity and gene expression in T1D, many of which map to T1D loci. For example, at the GLIS3 locus T1D variants mapped in a beta cell cCRE linked to GLIS3, both of which had altered activity in T1D. In total, genetics and single cell epigenomics together revealed novel insight into the regulatory programs, genes and cell types underlying T1D risk.