Moreover, the TLR4 signaling pathway also influences interferon (IFN)-β responsiveness in patients with MS where IFN responders exhibit a significantly lower baseline expression of the TLR4-negative regulator, interleukin (IL)-1 receptor-associated kinase (IRAK)3, compared to non-responders, resulting in proving the critical roles of TLR2 or TLR4 incorrect responses in MS etiology (17). This evidence concerns the gene TLR4 and myeloid sarcoma.