Increasing evidence suggests a key role for neuroinflammation in epilepsy.133 After status epilepticus, PVMs and microglia expressed chemokine ligand 2 (CCL2) and recruited circulating monocytes expressing CCR2.12 Another study also confirmed persistent PVM activation in the hippocampus of epileptogenic humans and rats.134 The expression of CD68, CCL2 and the PVM marker CD163 correlated with the onset of the first insult and the incidence of spontaneous seizures, suggesting that these proteins contribute to epileptogenesis and epilepsy progression. The gene discussed is CD163; the disease is epilepsy.