ACV treatment was also unsuccessful in rescuing the damage phenotype of oligodendrocytes and demyelination defects associated with increased MLKL suggesting that standalone ACV therapy in response to virus‐induced MLKL activation and upregulation is insufficient and while the initial trigger in the pathology may have been the virus, the tight regulation of the MLKL‒OPTN axis protects against this severe neuropathy (Figure 6H,J). Here, MLKL is linked to neuropathy.