CaMKII activity correlates with sustained increase in cytosolic Ca2+ (Fig. 4A) and is known to be a downstream target of P2X7 receptor signaling and to mediate neuronal cytotoxicity in the context of I/R, stroke and neurodegenerative diseases, pathologic conditions where ATP-mediated excitotoxicity is known to play a prominent role29, 30. Here, CAMK2G is linked to Stroke.