Although anti-SSA or anti-SSB play an important role in pSS pathogenesis [6, 8, 9], whether those pSS patients who are negative for anti-SSA and anti-SSB (non-antinuclear antibodies (ANA), which we termed seronegative pSS) share same pathogenesis mechanisms and clinical characteristics with those who are positive anti-SSA or anti-SSB (which we termed seropositive pSS) still needs to be explored. This evidence concerns the gene TRIM21 and peeling skin syndrome.