In fact, IFN-I upregulation has been shown in both peripheral cells and salivary glands from pSS patients, the so-called IFN signature [38], and it has been postulated that a primary viral infection induces IFN-I synthesis in salivary glands with subsequent activation of the adaptive immune response resulting in autoantibody production against RNA binding proteins, for example, SSA, SSB, RNP, which are interferogenic complexes that stimulate CD123hi/CCR6+/IDO+ cells to synthesize IFN-I, although this does not distinguish clinical disease activity. The gene discussed is CCR6; the disease is viral infectious disease.