This reinforces the role of NonO in decreasing the inflammatory response, given that IL-17 is known primarily for its ability to initiate a potent inflammatory response that includes the IL-1β, IL-6, and tumour necrosis factor [26]; and IL-23 activates macrophages and maintains chronic autoimmune inflammation via the regulation of T memory cells, especially T helper-type 17 cells, which are known to be one of the main players in orchestrating the adaptive immune response in MS [27,28]. This evidence concerns the gene NONO and myeloid sarcoma.