Moreover, disruption of CaMKIIβ expression has been linked to neurodevelopmental and synaptic plasticity alterations, and Cho et al. (2007) documented that transgenic mice, which expressed an elevated CaMKIIβ activity, displayed reduced LTP in the perforant path of the dentate gyrus (Cho et al., 2007), thus suggesting its potential impact on brain diseases. The gene discussed is CAMK2B; the disease is brain disorder.