Over half of all pSS patients exhibit an IFN signature, and these patients typically present higher titers of anti–Sjögren’s-syndrome-related antigen A (SSA/Ro) and anti–Sjögren’s-syndrome-related antigen B (SSB/La) autoantibodies and higher disease activity as measured by the European League Against Rheumatism Disease Activity Index (ESSDAI) [18]. The gene discussed is TRIM21; the disease is peeling skin syndrome.