Also consistent with the voltage-clamp studies, acute (ex vivo) pharmacological inhibition of all of the proposed signaling molecules in the TNFR1–JAK2–FGF14–Nav1.6 pathway ameliorated the hyperexcitability phenotype induced by infection, demonstrating that disruption of the signaling network is sufficient to block features of eCM related to neuronal excitability. The gene discussed is TNFRSF1A; the disease is infection.