In the present study, we demonstrate that JMS effectively inhibits melanin synthesis, tyrosinase activity, and melanogenesis-related protein expression levels through the CaMMKβ-AMPK (calcium/calmodulin-dependent protein kinase β-5′ adenosine monophosphate-activated protein kinase) pathway in B16F10 melanoma cells. The gene discussed is PRKAA1; the disease is melanoma.