Furthermore, it should be noted that the transgenic mouse models previously used to demonstrate the disease-modifying effects of Kv1.3 blockade (i.e. APP/PS1 and 5 × FAD mice) do not reflect the majority of clinical AD cases, i.e. sporadic AD, that occur in elderly humans (without excessively elevated, lifelong cerebral amyloid precursor protein (APP) expression or Aβ production) [20]. Therefore, to enhance the translational potential of Kv1.3 blockers in AD, their effectiveness in a mouse model of sporadic AD needs to be assessed. This evidence concerns the gene KCNA3 and Alzheimer disease.