Although the etiology of pSS is not fully understood, numerous studies have reported that T cells and B cells are the primary sources of proinflammatory cytokine production and autoantibody secretion, promoting the development of pSS by producing various autoantibodies and inflammatory factors, including anti-nuclear antibody (ANA), anti-SSA, and anti-SSB (20,21). The gene discussed is SSB; the disease is peeling skin syndrome.