NFKB1 and Cerebral ischemia: While the molecular mechanisms underlying the effects of TMS are not fully understood, in models of cerebral ischemia, TMS has shown the ability to modulate neuroinflammation through inhibition of NF-kB and promotion of microglia M2 polarization [91], as well as antioxidant effects through upregulation of antioxidant enzyme transcription factors [92], making TMS theoretically a useful intervention early in the acute phase of TBI.