Circulating IL-35 is typically upregulated in AP, functioning through STAT1/STAT4 signalling to suppress effector T-cell proliferation, inhibit Th1/Th17 differentiation, and promote expansion of regulatory T and B cells, thereby limiting pro-inflammatory cytokine release (e.g., TNF, IL-6, IL-17) and reducing local and systemic inflammation. The gene discussed is STAT1; the disease is alkaline phosphatase measurement.