CaMKII (Ca²⁺/calmodulin-dependent protein kinase II; EC 2.7.11.17) is a serine/threonine kinase with a broad range of substrates, and it is found in most tissues, but it is present in especially high concentrations in neurons. In mammals, the kinase is encoded by four genes, α, β, γ, and δ, with the α and β isozymes predominant in the brain. CaMKII monomers assemble into a large holoenzyme. Monomers of different isozymes are able to coassemble, allowing for a large number of possible holoenzyme compositions, existing of 8-12 subunits[1]. CaMKII is involved in many signaling cascades. Neuronal CaMKII regulates important neuronal functions, including neurotransmitter synthesis, neurotransmitter release, modulation of ion channel activity, cellular transport, cell morphology and neurite extension, gene expression, and synaptic plasticity. Moreover, its activity is required for induction of long-term potentiation (LTP) in the CA1 region of the hippocampus. Since defects in LTP often accompany impairments in spatial learning, and animals that lack the αCaMKII isozyme do not learn normally in such tasks, CaMKII is frequently referred by as an important mediator in the process of learning and memory. Furthermore, misregulation of CaMKII is linked to Alzheimer’s disease, Angelman syndrome, and heart arrhythmia[2].