We observed in this work that inhibition of endogenous 14-3-3 function with difopein or BV02 noticeably rescued disease-related Eag1 degradation by Cul7, consistent with the idea that 14-3-3 regulation of Eag1 protein homeostasis may play a significant role in the pathophysiology of ZLS. This evidence concerns the gene YWHAQ and Zimmermann-Laband syndrome.