An early event in pathogenesis of AP is activation of NOD-like receptor family pyrin domain containing 3 (NLRP3), nuclear factor kappa-b (NFκB), and receptor interacting protein (Mayerle et al. 2019) (RIP3) receptors, which triggers cellular death, along with massive release of damage-associated molecular patterns (DAMPs) and inflammatory cytokines (such as interleukin-1β (IL-1β) and IL-6). Here, NLRP3 is linked to alkaline phosphatase measurement.