Prior studies have shown that NSC treatment leads to increased levels of BDNF, GDNF, NTF3, VEGF, and other neurotrophic factors which have demonstrated neuroprotective and regenerative effects in both rodent and pig stroke models.5,42 The data in this study further support the theory that increased NSC survival enhances neuroprotective and regenerative signaling as iNSC treatment without the Tan IIA-NP pretreatment resulted in a statistically significant increase in endogenous neuron survival and a decrease in immune cell and reactive astrocyte activation relative to PBS control pigs. The gene discussed is BDNF; the disease is stroke disorder.