Currently, it is widely accepted that after the upregulation of IL-23R, IL-23 signaling activates STAT3 through JAK2/ TYK2 and then mediates the transactivation of RORγt to induce the differentiation of pathogenic Th17 cells and the production of proinflammation cytokines, including IL-17A, IL-17F, IL-22, GM-CSF, and TNF-α, thereby driving inflammatory and autoimmune diseases [91]. The gene discussed is IL37; the disease is autoimmune disease.