Furthermore, the increased IL-17RA+ and IL-23R+ Th cells populations in SLE patients may be attributable to their shared molecular signaling pathway as the binding of IL-23 with its receptor complex activates STAT3 signaling in Th17 cells leading to IL-17 production through differentiation of Th17 cells (45, 46). The gene discussed is IL23R; the disease is systemic lupus erythematosus.