Combining TMS with BMSCs displayed a more efficient recovery in rats with spine injury in comparison with monotherapy by reducing neuronal apoptosis, increasing neurotrophic expression levels (GAP-43, NGF, BDNF), and downregulating the expression of glial fibrillary acidic protein (GFAP) [125], the marker of astrocytic activation mediating glial scar formation which is also released into the bloodstream after brain tissue damage and is associated with stroke severity [126,127]. The gene discussed is GAP43; the disease is Stroke.