Receptor activation inhibits macrophage nuclear factor kappa-light-chain-enhancer of activated B cells nuclear translocation[62] and promotes STAT3-dependent IL-10 secretion.[63] This pathway has shown therapeutic potential in autoimmune disease clinical trials, where α7 nicotinic acetylcholine receptor agonists have demonstrated the capacity to suppress Th17 cell differentiation while promoting Th2 polarization.[64]. This evidence concerns the gene STAT3 and autoimmune disease.