These reductions in PN number, dendritic branch complexity, and spine density (Fig. 3J) suggest that TLR4 is involved in maintaining PN survival, dendritic growth and plasticity, and spine dynamics, and further that a TLR4 signaling deficits may contribute to ataxia by impairing synaptic integration and PN output. The gene discussed is TLR4; the disease is cerebellar ataxia.