A cohort study reported that 23.2% of AP patients had significantly elevated titers of Coxsackievirus B or mumps virus antibodies.[16] Microbial infections or autoantigens can activate the immune system of the body, triggering a potent inflammatory cascade response.[17] Research has shown that inflammatory mediators are crucial for the occurrence and development of AP, among which the release of pro-inflammatory cytokines such as TNF-α, IL-9A and IL-8 can lead to an amplified inflammatory cascade effect.[18–20]. The gene discussed is TNF; the disease is alkaline phosphatase measurement.