Together with the knowledge that the STING pathway is critical for the production of IFN-β [15,17,22,23,26,27], and its direct activation showed promising results in the EAE model [30,31,32], it is likely that the STING/IFN-β-signaling pathway could account for the lower endogenous expression levels of IFN-β and IFN-dependent genes underlying the pathophysiology of MS, as described by others [20,40,41]. Here, STING1 is linked to myeloid sarcoma.