In a 2013 review by G Nocturne and X Mariette of the pathogenesis of SS (26), three key steps were identified based on the initial genome-wide association study (GWAS): aberrant activation of the innate immune response, especially through the interferon (IFN) and NF-κB pathways, atypical recruitment to lymphoid follicles mediated by CXCR5, and T cell activation with ascending HLA susceptibility along the IL-12–IFN-γ axis. This evidence concerns the gene NFKB1 and synovial sarcoma.