In the period of initiation, pSS is a Th1-dominated disease, leading to the high levels of IFN-γ and its related cytokines (IFNα/β and IL-12) in pSS patients.[9] IL-18 is also able to work synergistically with IL-12 to activate Th2 cells, Th17 cells, NK cell, etc[37] and produce high levels of autoantibodies (including RF, IgG, IgA, anti-Ro and anti-La, etc)[38,39] and the fibrosis of exocrine glandular tissue.[39,40] Simultaneously, IL-18 induced the overexpression of IL-17 in pSS patients,[41–43] which may be considered as an additional inducer of autoantibodies. The gene discussed is CALR; the disease is peeling skin syndrome.