into polygenic architectures (see below) by identifying tissue-specific functional annotations that are enriched for causal disease signals. This can also be achieved by conducting fine-mapping without integrating functional annotation data (typically under a single causal variant assumption) and then overlapping the resulting credible sets with functional annotation data to assess enrichment62–64. Future integrative methods could increase fine-mapping resolution by integrating probabilistic functional annotations (e.g., ChIP-seq peak intensity) or modeling the strength of association between SNPs and chromatin marks in population-based studies65,66.
