More specifically, B cell key pathogenic features in SLE include the following: (i) a hyperactive profile with increased antigen presentation capability; (ii) expanded populations of plasmablasts, memory, double-negative memory, and transitional cells; (iii) aberrancies in both pro- and anti-inflammatory cytokine secretion, highlighted by increased interleukin-10 (IL-10), IL-6, IL-4, and tumor necrosis factor–β (TNF-β) and decreased IL-2 production; and (iv) increased secretion of pathogenic autoantibodies (15, 18, 19). This evidence concerns the gene IL2 and systemic lupus erythematosus.