In the pathogenesis of EAE, mimic the MS in human, both Th1 and Th17 cells, also known as IFN-γ and IL-17A-producing CD4 T helper cells, respectively, are critically immunopathogenic players in the initiation and progression of EAE followed by neuronal demyelination in the CNS, consequently leading to the ascending paralysis of the tail as well as limbs of mice [21,22,23,24]. Here, IFNG is linked to myeloid sarcoma.