However, in a mouse model of EAE, used to emulate MS disease progression in mice, disrupted FKN signaling through the CX3CR1M280 SNP, exacerbated EAE progression, including microglia dysfunction, and subsequent inflammation, demyelination, and degeneration of neurons (Cardona et al., 2018). The gene discussed is CX3CL1; the disease is myeloid sarcoma.