In a mouse model of multiple sclerosis, IL-1β-mediated inflammation was found to enhance glutamatergic transmission during the early phase of the disease (Centonze et al., 2009; Rossi et al., 2012, 2014; Mandolesi et al., 2013), through modulating vanilloid 1 channels in hippocampus (Rossi et al., 2012), downregulating the glutamate–aspartate transporter/excitatory amino acid transporter 1 (GLAST/EAAT1) in the cerebellum (Mandolesi et al., 2013, 2017), and by activating the apoptotic cascade through p53 activation (Rossi et al., 2014). The gene discussed is IL1B; the disease is multiple sclerosis.