IFNA1 and systemic lupus erythematosus: As the signature of SLE, excessive production of type I IFN (especially IFN-α) substantially contributes to SLE pathogenesis by triggering the activation and expansion of autoreactive immune cells, promoting autoantibodies production and inflammatory cytokines release, hence leading to the formation of nucleic acid-protein immune complex and perpetuating the autoreactive immune response.