Considering that the E251K mutation in OSM-3 is analogous to the E253K mutation in KIF1A, future studies will ascertain whether the inhibition of jbts-26 can ameliorate neuronal defects induced by KIF1A E253K, potentially unveiling a novel therapeutic target for intervening in KIF1A E253K-associated neurological disorders. Here, KIF1A is linked to nervous system disorder.