For instance, in the case of autoimmune diseases, such as multiple sclerosis or experimental autoimmune encephalomyelitis, neutrophils are known to be attracted by the release of CXCL1, CXCL2, and CXCL5, which are in turn stimulated by different molecules, such as IL-17 or IFN-γ (Christy et al., 2013; Simmons et al., 2014). This evidence concerns the gene IFNG and experimental autoimmune encephalomyelitis.