{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T23:14:54Z","timestamp":1790378094328,"version":"4.1.0"},"reference-count":11,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2019,5,4]],"date-time":"2019-05-04T00:00:00Z","timestamp":1556928000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clinical Case Reports"],"published-print":{"date-parts":[[2019,6]]},"abstract":"<jats:title>Key Clinical Message<\/jats:title><jats:p>Different mutations in glutamate receptor ionotropic delta 2 (GRID2) gene cause cerebellar ataxia in human. We report the largest homozygous deletion of the GRID2 gene reported to date, most probably causing complete loss of the gene product. 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