Although a direct study has not yet confirmed the link between CaV2.2 and neuropathic pain in MS/EAE, the involvement of this channel in EAE pathophysiology, its role in neuropathic pain, together with the use of N-type Ca2+ channel blockers in the treatment of chronic pain in MS patients (182–184), point toward the need for further investigations to determine how CaV2.2 plays a role in EAE-associated pain. Here, CACNA1B is linked to myeloid sarcoma.