There is evidence that a deficiency in the cytotoxic capacity of CD56bright NKs in MS patients correlates with MS attacks and with the development of new inflammatory lesions [70,71], even though CD56bright NK frequencies in untreated MS patients are similar to those in HCs, but they expand in response to certain treatments, such as DMF or IFN-β [68,72]. This evidence concerns the gene IFNB1 and myeloid sarcoma.