Abstract
Loss-of-function mutations in Janus kinase 3 (JAK3) are an underlying cause of severe combined immunodeficiency (SCID), whereas hyperactive JAK3 mutants have been identified in hematolocigal malignancies.1–3 In this issue of Blood, Elliot et al place JAK3 again under the magnifying lens and describe novel gain-of-function mutations in the FERM (Founding members: band 4.1, Ezrin, Radixin, and Moesin) domain of JAK3 in adult patients with T-cell leukemia/lymphoma (ATLL).4
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