These complexes can deposit in tissues, initiating an inflammatory response and resulting in damage to multiple organs (46); (iii) The increased release of inflammatory mediators, such as type-I interferons (type-I IFN), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), contributes to the inflammatory processes and tissue damage associated with SLE (47); (iv) Circulating immune complexes (ICs) in the patient’s serum trigger the complement system, leading to the depletion of significant amounts of complements C3 and C4. The gene discussed is IL6; the disease is systemic lupus erythematosus.