In patients with Sjögren’s syndrome, the S1P/S1P1 axis has been shown to contribute to disease pathogenesis through increased expression of S1P1 in salivary gland mononuclear cells and increased S1P-driven IFN-γ production by CD4+ T cells, resulting in enhanced IFN-γ-mediated Fas expression and Fas-dependent apoptosis of salivary gland epithelial cells [22]. This evidence concerns the gene IFNG and Sjogren syndrome.