As we know, excess levels of IL-1β, IL-6, and TNF-α induced by activated inflammatory cells (e.g., eosinophils, macrophages, mononuclear phagocytes, neutrophils) will lead to the damage of cells and tissues, which eventually cause the inflammation-associated diseases; for example, rheumatoid arthritis, chronic hepatitis, and macrophages play an important role in regulating several immunopathological conditions and inducing overexpression of the proinflammatory mediators of the inflammatory process [24, 25]. This evidence concerns the gene IL1B and chronic hepatitis.