Analyses of patient biopsies and mouse models of SS have identified a large number of immune signaling pathways that may underlie the disease, such as activation of IFNγ producing T-helper 1 (Th-1) [4,5] and IL17 producing T-helper 17 (Th-17) CD4+ T cells [6,7], B cell activation [8,9], upregulation of pro-inflammatory cytokines (e.g., IL1, IL6, and IL17) [6,7,10,11], ligation of Toll-like receptors expressed on infiltrating immune and ductal epithelial cells [12,13], phosphorylation of signal transducer and activator of transcriptions (STATs) [13], and signaling via the NF-κB pathway [13]. This evidence concerns the gene IFNG and synovial sarcoma.