The use of preclinical animal disease models, as well as human sample analyses, revealed that neutrophils have a wide range of effector functions that contribute to MS pathogenesis, including secretion of inflammatory mediators and enzymes such as IL-1 [105], elimination and phagocytosis of myelin (as debris), discharge of neutrophil extracellular baits, generation of reactive oxygen species (ROS) [106, 107], breakdown of the BBB, and production and introduction of autoantigens [108]. Here, IL1B is linked to myeloid sarcoma.