These inflammatory mediators, which are produced by immune cells, create a complex interaction network that further influences immune cell function and activity.[14] Targeted therapeutic strategies, such as anti-IL-1β treatment, have shown promise for improving sepsis outcomes.[15,16] Inflammatory proteins, including tumor necrosis factor (TNF-α), IL-6, and IL-1β, are integral to the inflammatory response in sepsis, driving immune cell activation and migration and modulating vascular permeability and coagulation.[17–20]. The gene discussed is IL1B; the disease is Sepsis.