KCNA3 and systemic lupus erythematosus: Nicolaou et al. [29] reported a defect in Kv1.3 trafficking to the immunological synapse (IS) of SLE T cells that might contribute to the Ca(2+) defect and proposed that Kv1.3 trafficking abnormalities contribute to the altered distribution of Ca(2+) signaling in SLE T cells, with these defects explaining in part the T cell hyperactivity and dysfunction documented in SLE patients.