As an inflammatory process, AP results in excessive leukocyte activation and increased migration of neutrophils to the inflamed area, with a consequent release of pro-inflammatory mediators including interleukins (IL-6, IL-8, IL-15, IL-33, and IL-17), procalcitonin and tumor necrosis factor-a (TNF-α) [8–13]. The gene discussed is IL17A; the disease is alkaline phosphatase measurement.