TNFRSF1A and infection: Compared to AAV-shCTRL treatment, AAV-shFGF14 treatment mitigated the hyperexcitability phenotype caused by P. chabaudi infection and restored action potential firing back to a level comparable to the uninfected control condition (Fig. 4D, Additional file 1: Table S4), which demonstrates that in vivo modulation of the TNFR1–JAK2–FGF14–Nav1.6 signaling network at the level of FGF14 is sufficient to block the perturbations in neuronal excitability caused by infection.