Deletion of the TRPV1 channels in TRPV1 knockout mice exacerbated the defects of glutamate transmission occurring in the peak phase of EAE, and attenuated alterations in the GABA synapses in the chronic phase of EAE, in consistency with the dual effect of TRPV1 deletion on the motor deficits of EAE mice, suggesting a potential therapeutic target of TRPV1 for MS [54]. Here, TRPV1 is linked to myeloid sarcoma.