Historically, depression has been correlated with monoamine bioavailability alterations at the synaptic level [4]; however, some studies have associated the development of depression with ion channel alterations, including AMPA and NMDA type glutamate receptor, GABA-A receptor, potassium channels, and calcium channels [5,6,7,8]. The gene discussed is KCNA3; the disease is depressive symptom measurement.