Epilepsy is a seizure causing disorder due to an abnormal brain activity as consequence of hyperexcitability. The K+ currents are important for preventing this hyperexcitability. The M-current is an important K+ current constituted out of the K+ channels named Kv7.2 and Kv7.3. It is important that this M-current does not decrease over time and becomes inactive, known as channel inactivation. The difference between Kv7.2/3 and the other Kv channels is the absence of inactivation, but the reason behind this is still not clear since the mechanism of Kv7 channel inactivation is still not fully clarified. Understanding how these channels work, including the inactivation mechanism, is important for analysing the effects of genetical mutations in these channels and the impact on the M-current. A remarkable difference between Kv7.2/3 and other Kv7 channels is the presence of a Valine residue in the pore domain. Therefore this Valine residue’s role in the working mechanism of Kv7.2 and Kv7.3 has been elucidated. Although, the results did not show that this residue is the explanation behind the difference in working mechanism between Kv7.2/3 and Kv7 channels, they did show that the pore mutations can induce domain inactivation that consequently influences the working of the M-current. The inactivation process in the Kv7 channels is a neglected property of the current, but most likely a potential driver for the pathogenesis of epilepsy and a potential mechanism for therapeutic intervention. Therefore it is important to study and understand the inactivation mechanism in order to understand and treat epilepsy. This can be a contribution to public health, pharmaceutical industry and stakeholders such as patients.