Sepsis compromises immune cell functionality both directly and indirectly via damage-associated molecular patterns (DAMPs), including proinflammatory cytokines (IL-1β, TNF-α, IL-6) (40, 41), iNOS (42, 43), reactive oxygen species (ROS) (44), heat shock proteins, HMGB1, histones, activated complement components, and mitochondrial DNA. This evidence concerns the gene IL1B and Sepsis.