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. 2022 Jan 20;5:80. doi: 10.1038/s42003-022-03031-6

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© The Author(s) 2022

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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Fig. 5 — a 18 gene-disease associations with suggestive significance (P_{GBJ conditional} < 0.05; i.e., after multiple-gene-conditioned fine-mapping analysis) are enriched in the “calcineurin-dependent NFAT signaling in leukocytes” pathway (comprising 55 genes; Methods), showing genetically altered gene expression for SCZ, CD, or UC compared to healthy controls. PPP3CA encodes the catalytic subunit calcineurin A; FKBP1A (also known as FKBP12) encodes a cis-trans prolyl isomerase that binds the immunosuppressant FK506 (tacrolimus). b The calcineurin inhibitor tacrolimus, used against various inflammatory diseases and as an immunosuppressant in organ-transplanted PSC-IBD patients, prevents NFAT signaling by binding to FKBP1A and causes inhibition of calcineurin. The reduced genetic expression of PPP3CA that we identified in intestinal and brain tissues causes an increased risk of SCZ and CD (Table 2). Raw data of this figure can be found in Supplementary Data 18.