The mechanisms underlying the glandular dysfunction in SS are not fully understood, but potential mechanisms include T-cell-mediated destruction of glands, the presence of anti-muscarinic 3 receptor autoantibodies, modified aquaporin-5 (AQP5) distribution, and the presence of anti-AQP5 autoantibodies [8,9,10,11,12]. Here, AQP5 is linked to synovial sarcoma.