Therefore, we speculated that CD161, as an inhibitory receptor of NK cells, decreased on the surface of CD56+ NK cells in pSS patients, which weakened the inhibition on NK cell function, and led to the increased secretion of cytokines such as IFN‐γ, promoted the activation and proliferation of B cells, and produced more auto‐antibodies and immunoglobulins in pSS patients. This evidence concerns the gene NCAM1 and peeling skin syndrome.