IKBKB and myeloid sarcoma: Together, our results show that neuronal TNFR1 and IKKβ promote neuroinflammation and the onset of demyelination in mouse models of MS and that neuronal TNFR1 is additionally required for axon damage, OLG loss, and induction of glial cell autophagy in white matter lesions during CPZ demyelination, possibly by increasing neuronal oxidative stress.