Remember, in the Glucagon signal transduction pathway that initiates Glycogen breakdown, the canp acts as a secondary messenger that is used to basically activate the inactive protein kinase Apka into the active version of PKA. But now that we are no longer producing cyclic Amp as a result of the inactivation of the adenaline cyclist, and because the CA and P are being transformed into A and P, the PKA is no longer activated. Now let's move on to D. So in D and E, what we basically want to do is we want to inactivate the phosphoralase kinase that is needed to activate the Glycogen phosphorase and we also want to inactivate the Glycogen phosphorase that is ultimately needed in step one of Glycogen breakdown. So let's focus on D. So essentially, in order to inactivate the phosphoralase kinase, what happens is the PKA must phosphorylate the alpha subunits of Asphylase kinase. So the same PKA that is used to activate phosphorylase kinase is also actually used to inactivate phosphorase kinase. Remember when PKA phosphorylates the beta subunits, that activates this, but when PKA phosphorlates the alpha subunits, that causes the phosphorylase kinase to become a good substrate for another protein known as PP one, which stands for protein phosphatase one.