Therefore, Atg5-mediated alterations in autophagy may impair the activation of DCs through the immune complexes present in SLE patients, thus preventing the production IFNα and the activation of NF-κB, a pathway involved in the transcription of Th1-promoting cytokines, TNFα and other proinflammatory mediators. The gene discussed is IFNA1; the disease is systemic lupus erythematosus.