Systemic lupus erythematosus (SLE) is a complex systemic autoimmune disease characterized by elevated type I interferon (IFN) production, a break of immune tolerance to self-antigens, persistent production of pathogenic autoantibodies, complement activation, and immune complex (IC) deposition resulting in inflammation and end organ damage [1]. Here, IFNA1 is linked to systemic lupus erythematosus.