In MS lesions, treatment with omega‐conotoxin (a selective Cav2.2 inhibitor) reduced axon and myelin damage (Gadjanski et al. 2009), whereas in MOG peptide EAE, a1B null mice have reduced clinical signs and less demyelination (Tokuhara et al. 2010); and treatment with ziconotide‐a (selective Cav2.2 blocker) reduced clinical signs and neuroinflammation (Silva et al. 2018). The gene discussed is MOG; the disease is myeloid sarcoma.