Neural precursor cell (NPC) transplantation boosts the endogenous neurogenic response after stroke. NPC proliferation within the SVZ is augmented after stroke leading to the generation of newly formed neuroblasts that migrate along vessels toward gradients of chemokines that are produced locally by glial and inflammatory cells (e.g., CCL2, SDF1-α, and EPO). The bystander effects of transplanted NPCs depend on the release of several factors (e.g., BMP, SHH, NGF, BDNF, CNTF, GDNF, NT-3, and VEGF) that can directly increase cell proliferation within the SVZ, potentiate neuroblasts migration, and augment peri-ischemic angiogenesis. Transplanted NPCs can also positively affect the differentiation of endogenous neuroblasts and plasticity within the ischemic tissue (via the secretion of NGF, BDNF, CNTF, GDNF, NT-3, MMPs, TIMPs, CSPGs, TN-C, VEGF, TSP1-2, Slit), or directly differentiate into post-mitotic neurons, astrocytes, or oligodendrocytes. Most importantly, transplanted NPCs secrete a plethora of soluble molecules that modulate the activation of host microglia/macrophages (e.g., BMP, LIF, NO, PGE, HO-1, VEGF, TN-C), thus modifying the release of inflammatory mediators that inhibit (e.g., TNF-α, IFN-γ, IL1β, IL6) or increase (e.g., TNF-α, IGF1) endogenous neurogenesis. Green dots represent mediators secreted by inflammatory cells.