Some even argue that blocking increased Kir4.1 activity could potentially lead to severe epilepsy, ataxia, and deafness in humans.[28] Interestingly, a very recent study suggests that a dysconnection in K+ shuttling between axonal Kv7 and oligodendroglial Kir4.1 contributes to the pathogenesis of MS, as evidenced by MS‐like symptoms observed in Kir4.1‐deficient mice.[29] Therefore, the activation or inhibition of Kir4.1 activity remains a widely challenging aspect of strategic MS treatment. This evidence concerns the gene KCNJ10 and Ataxia.