These results suggest that the inhibition of Cdk activity appears to be due in part to increased levels of Cdk inhibitors.To determine whether AMPK inactivation is a critical factor in CompC-induced G2/M cell cycle arrest in B16-F1 melanoma cells, these cells were transfected with AMPKα1/2 siRNA for 48 h, followed by treatment with 10 μM CompC for 16 h. This evidence concerns the gene PRKAA1 and melanoma.