>*"An example is the SCN2A gene that is strongly associated with epilepsy. It encodes sodium ion channels and mutations in this gene can lead to hyperexcitability. So this is why epilepsy is typically treated with a sodium channel blocker or gaba agonist to tone down the glutamatergic hyperexcitability."* That makes a lot of sense. So how do you propose this works in developmental stuttering (i.e., childhood-onset stuttering)? And in what way should developmental stuttering be addressed through genetics exactly? (which would lead to stuttering remission e.g., in the same way how [this ](https://www.google.nl/books/edition/The_Perfect_Stutter/_u8vEAAAQBAJ?hl=en&gbpv=1&dq=the+perfect+stutter&printsec=frontcover) Phd researcher achieved a 10 year stuttering remission, page 356)