TLR4 and cerebellar ataxia: Thus, weakening of ER–mitochondria tethering associated with TLR4 knockout may explain the mitochondria damage in PNs as well as the reduced number of PNs, the diminished arborization of PN dendrites, and the lower spine density on PN dendrites in TLR4PKO mouse cerebellum, ultimately resulting in abnormal PN firing and cerebellar ataxia-like behaviors.