These data, in addition to the observation from animal models with RA (115) and that the TIGIT expression levels on human NK cells was associated with functional heterogeneity among healthy individuals leading to different susceptibilities to infection, autoimmune disease, and cancer, support the importance of TIGIT as a powerful negative regulator of NK cells in SLE, whose activation could represent a potential therapeutic strategy (116). The gene discussed is TIGIT; the disease is cancer.