CAMK2G and Stroke: Mechanistically, tat-CN21 and tat-AIP can both block Ca2+/CaM-stimulated activity of CaMKII and the Ca2+-independent autonomous CaMKII activity during the insult, whereas KN93 only inhibits Ca2+/CaM–stimulated CaMKII activity effectively, suggesting that the autonomous activation of CaMKII may be a promising drug target for post-stroke neuroprotection.