The study by Kay et al. [20] suggests that the initial inflammatory response in AP develops as naive Th17 cells are generated in response to macrophage-derived IL-6 [20], whereas the development of SAP occurs as a result of Th17 response with a greater pathogenic potential (IL-23 induced), probably due to dysfunctional autophagy or the inability of monocytes to mount an adequate IL-10 anti-inflammatory response due to anergy [20]. The gene discussed is IL6; the disease is alkaline phosphatase measurement.