Store-operated calcium entry (SOCE) by the calcium release-activated calcium (CRAC) channel is a key module of the molecular machinery underlying antigen receptor signaling in T-lymphocytes. Loss of function or expression of one of the core components of the CRAC channel complex, STIM1 and Orai1, leads to severe immunodeficiency in both mice and humans. However, the contribution of the regulatory factor SARAF, integral to the CRAC channel complex, remains unclear in immune function. To address this gap, utilizing mice and cells genetically lacking SARAF this proposal aims to explore the role of SARAF in adaptive immunity and calcium signaling in T-lymphocytes.