As JNK, among the three MAPKs (JNK, p38 and extracellular signal‐regulated kinase), was shown to be the prominent downstream target of hypothalamic DUSP8 signaling toward GRser226 phosphorylation, the authors studied the involvement of JNK by using mice with codeletion of Jnk1 and Dusp8 (Jnk1‐Dusp8‐dKO), and found that the exacerbation of HFD‐induced glucose intolerance and hypercorticosteronemia observed in HFD‐fed Dusp8‐KO mice were abrogated by additional deletion of Jnk1, suggesting that JNK mediates DUSP8 effects on systemic metabolism. The gene discussed is MAPK8; the disease is Glucose intolerance.