Although no definite focal demyelination or inflammation could be detected in the CNS of PGC-1α-deficient animals as seen in EAE, the knockout mice develop dysmyelination [140] and oligodendroglial and intramyelinic vacuolation [102,103] strikingly reminiscent of that seen in mice treated with the toxin cuprizone used in the in vivo modeling of MS [141]. Here, PPARGC1A is linked to myeloid sarcoma.