Due to the potential pathogenetic role of S100A proteins in pSS and in the production of other inflammatory mediators, including IL-1 family proteins, we validated the expression of S100 A7 in 19 additional pSS patients and 8 controls confirming that S100A7 expression was significantly higher in patients with high focus/low flow (305.6 ± 174 ng/ml vs 11 ± 14 ng/ml vs 75.7 ± 21.6 ng/ml, p = 0.000) (Fig. 6b). The gene discussed is S100A1; the disease is peeling skin syndrome.