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Among MPNs, Essential thrombocythemia (ET), Polycythemia Vera (PV) and Myelofibrosis (MF), are driven by mutations that activate the JAK\u2013STAT signalling pathway. Somatic mutations of calreticulin (CRT), an endoplasmic reticulum (ER)\u2010localized lectin chaperone, are driver mutations in approximately 25% of ET and 35% of MF patients. The MPN\u2010linked mutant CRT proteins have novel frameshifted carboxy\u2010domain sequences and lack an ER retention motif, resulting in their secretion. Wild type CRT is a regulator of ER calcium homeostasis and plays a key role in the assembly of major histocompatibility complex (MHC) class I molecules, which are the ligands for antigen receptors of CD8<jats:sup>+<\/jats:sup> T cells. Mutant CRT\u2010linked oncogenesis results from the dysregulation of calcium signalling in cells and the formation of stable complexes of mutant CRT with myeloproliferative leukemia (MPL) protein, followed by downstream activation of the JAK\u2013STAT signalling pathway. The intricate participation of CRT in ER protein folding, calcium homeostasis and immunity suggests the involvement of multiple mechanisms of mutant CRT\u2010linked oncogenesis. In this review, we highlight recent findings related to the role of MPN\u2010linked CRT mutations in the dysregulation of calcium homeostasis, MPL activation and immunity.<\/jats:p>","DOI":"10.1111\/jcmm.17713","type":"journal-article","created":{"date-parts":[[2023,3,14]],"date-time":"2023-03-14T06:55:37Z","timestamp":1678776937000},"page":"1032-1044","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Effects of calreticulin mutations on cell transformation and immunity"],"prefix":"10.1111","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3611-9866","authenticated-orcid":false,"given":"Harini","family":"Desikan","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology University of Michigan Medical School  Ann Arbor Michigan 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