In the initial stage of sepsis, inflammatory cells such as macrophages and neutrophils are activated to produce a large number of pro-inflammatory cytokines, such as interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α), as well as reactive oxygen species lead to endothelial and epithelial damage, affect vascular permeability and heart function, and eventually result in tissue necrosis and organ failure [4]. Here, IL1B is linked to Sepsis.