On the other hand, T-Lymphocyte activation is SOCE-dependent, as illustrated by STIM1/ORAI1 deficient humans who exhibit lymphoproliferative defects and severe combined immunodeficiency (SCID), a phenotype consistent with SOCE-deficient mouse models, although murine STIM/ORAI proteins show a higher level of functional redundancy (9). The gene discussed is STIM1; the disease is severe combined immunodeficiency.