IL6 and myeloid sarcoma: Upon homeostatic dysregulation, microglia and CNS-infiltrated macrophages can be pushed towards an M1 pro-inflammatory phenotype to mediate secretion of TNFα, IL-12, IL-6, IL-23, and TGFβ at elevated levels, promoting TH1 and TH17 differentiation, which in turn provide feedback to facilitate M1 polarization, and ultimately leading to MS pathology (120, 121).