In agreement with the fact that PBN improves LTP/LTD defects in Tg hippocampal slices (Figure 3), our results show that the acute inhibition of Panx1 with PBN significantly reduces p38MAPK activation (Figure 5A), suggesting that Panx1 overactivity contributes to the neurotoxic signaling that leads to p38MAPK activation in AD. The gene discussed is PANX1; the disease is Alzheimer disease.