A mutant cell line expresses a constitutively active $G_{\alpha s}$ subunit coupled with a complete loss-of-function mutation in phosphodiesterase (PDE), resulting in chronically elevated intracellular cyclic AMP (cAMP) and hyperactivation of Protein Kinase A (PKA). If this cell line is treated with a physiological concentration of a ligand that normally binds to a $G_{\alpha i}$-coupled receptor (inhibitory to adenylyl cyclase), what is the predicted net effect on intracellular cAMP levels and downstream CREB phosphorylation?

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