As a negative regulator involved in innate immunity, along with induction of kinase activity of IRAK1/4 during infection, IRAK-M interacts with IRAK4 to induce transcription of downstream inhibitors such as A20, IĸBα, SOCS-1 and SHIP, to prevent radical immune pathology of the host [14, 18]. This evidence concerns the gene SOCS1 and infection.