Potential mechanisms of autonomic dysfunction in SS include T-cell infiltration and destruction of ganglions and nerves [28], cytokine-induced inhibition of neuropeptide secretion from nerve endings [29], immune complex-mediated inflammation (although few pSS patients in this study exhibited cryoglobulins and/or low C3 or C4, which might indicate immune complex deposition), and pathogenic autoantibodies targeting receptors relevant for autonomic functioning [30]. The gene discussed is C4A; the disease is peeling skin syndrome.