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. 2021 Oct 6;598(7879):129–136. doi: 10.1038/s41586-021-03604-1

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Extended Data Fig. 22 — a, Bar plot showing the percentage of cCREs identified in the current study with homologous sequences in the human genome (using reciprocal homology search) (Methods). b, Chromatin accessibility profiles for several neuronal and non-neuronal cell types, and posterior probabilities of association (PPA) for potential casual variants surrounding the homologous region in the mouse genome to a schizophrenia-associated locus. Grey bars highlight cCREs overlapping potential causal variants. rsID or hg19 coordinates of overlapped variants are labelled. ‘:D’ denotes that the alternative allele is a deletion; ‘:I’ denotes an insertion. Predicted positively correlated cCRE–gene pairs are shown in red arcs.