Several pathways are actually proposed to explain the aberrant immunity in SLE, focusing on the imbalance between production and clearance of apoptotic debris, activated innate and adaptive immunity, inflammatory cell recruitment and tissue injury mediated by the augmented synthesis of pro-inflammatory cytokines derived from activated macrophages (TNFα, IL-6, IL-8), T cells (IL-17) and B cells (IL-10 and IL-6 as a result of IL-21 costimulation), loss of T and B cell tolerance and, finally, excessive autoantibody synthesis partially dependent on a specific type I IFN signature [16,17,18,19]. The gene discussed is IL17A; the disease is systemic lupus erythematosus.