Furthermore, an abnormal activation of the NF-kB signaling pathway was observed in pSS monocytes (20), and the levels of pro-inflammatory mediators that are produced by monocytes and drive B cell activation, such as IL-6, type I interferon (IFN), B cell activating factor (BAFF), and chemokine C-X-C motif ligand 13 (CXCL13), are significantly increased in the inflamed tissues and circulation of pSS patients (21–24). The gene discussed is IFNA1; the disease is peeling skin syndrome.