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However, dysfunction of T cells, including exhaustion, is an inevitable obstacle for persistent curative effects. Here, the authors initially found that calcium signaling is hyperactivated via sustained tonic signaling in CAR\u2010T cells. Next, it is revealed that the store\u2010operated calcium entry (SOCE) inhibitor BTP\u20102, but not the calcium chelator BAPTA\u2010AM, markedly diminishes CAR\u2010T cell exhaustion and terminal differentiation of CAR\u2010T cells in both tonic signaling and tumor antigen exposure models. Furthermore, BTP\u20102 pretreated CAR\u2010T cells show improved antitumor potency and prolonged survival in vivo. Mechanistically, transcriptome and metabolite analyses\u00a0reveal that treatment with BTP\u20102 significantly downregulate SOCE\u2010calcineurin\u2010nuclear factor of activated T\u2010cells (NFAT) and glycolysis pathways. Together, the results indicate that modulating the SOCE\u2010calcineurin\u2010NFAT pathway in CAR\u2010T cells renders them resistant to exhaustion, thereby yielding CAR products with enhanced antitumor potency.<\/jats:p>","DOI":"10.1002\/advs.202103508","type":"journal-article","created":{"date-parts":[[2022,1,15]],"date-time":"2022-01-15T00:42:50Z","timestamp":1642207370000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":61,"title":["Inhibition of Calcium Signaling Prevents Exhaustion and Enhances Anti\u2010Leukemia Efficacy of CAR\u2010T Cells via SOCE\u2010Calcineurin\u2010NFAT and Glycolysis Pathways"],"prefix":"10.1002","volume":"9","author":[{"given":"Mi","family":"Shao","sequence":"first","affiliation":[{"name":"Bone Marrow Transplantation Center The First Affiliated Hospital Zhejiang University School of Medicine  Hangzhou Zhejiang 310003 China"},{"name":"Institute of Hematology Zhejiang University  Hangzhou Zhejiang 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