Moreover, given the structural simplicity of gallic acid, medicinal chemistry modifications to improve selectivity, efficacy and potency while still targeting the Kv1.1 VSD-binding site may lead to advances in ataxia therapy, which currently relies on repurposing epilepsy drugs such as carbamazepine, due to the previous lack of a potent and selective drug to restore mutant Kv1.1 function76. The gene discussed is KCNA1; the disease is cerebellar ataxia.