Ca2+/calmodulin-dependent protein kinase II alpha (CaMKII alpha) is an enzyme that adds phosphates to a variety of protein substrates to modify their functions. CaMKII alpha is enriched in the hippocampus, the memory center of the brain, and is believed to be an essential mediator of activity-dependent synaptic plasticity and memory functions. However, the causative role of the enzymatic activity of CaMKII alpha in such processes has not been demonstrated yet, because this enzyme has multiple protein functions other than the kinase activity. A Japanese research group, led by Dr Yoko Yamagata of the National Institute for Physiological Sciences, Japan, has successfully generated a novel kinase-dead mutant mouse of the CaMKII alpha gene that completely and exclusively lacks its kinase activity. They examined hippocampal synaptic plasticity and behavioral learning of the mouse, and found a severe deficit in both processes. They reported their findings in the Journal of Neuroscience, published on June 10, 2009.