The involvement of IRAK-4 in TLR7 and TLR9 signaling, coupled with the observation that dual inhibition of TLR7 and TLR9 in lupus-prone mice results in amelioration of disease symptoms, indicates that IRAK-4 may be a suitable therapeutic target for systemic lupus erythematosus (SLE) [26, 29]. This evidence concerns the gene TLR7 and systemic lupus erythematosus.