During acute inflammatory attacks in MS and EAE, pro-inflammatory cytokines (such as tumor necrosis factor (TNF); interleukin-1β (IL-1β)), released from activated microglia and astroglia as well as from infiltrating lymphocytes, trigger a progressive increase of the glutamatergic transmission and an impairment of the GABAergic synaptic response, leading to uncontrolled excitability and possibly to neurodegeneration (Centonze et al., 2009; Rossi et al., 2011, 2012, 2014; Mandolesi et al., 2012, 2013, 2017a; Nisticò et al., 2013; Mori et al., 2014a). This evidence concerns the gene TNF and myeloid sarcoma.