Almost 30 yr have passed since the discovery of the heptahelical transmembrane (TM) receptors and their connection to heterotrimeric G proteins and sequential signal flow to intracellular effectors (1–3). Many hormones, sensory stimuli, and neurotransmitters use this signaling system to convert chemical or physical information from the G protein-coupled receptor (GPCR) through a transducer (G protein) to an effector into an intracellular language that the cell can comprehend and to which it can respond. In the liver, epinephrine signals via the β-adrenergic receptor (AR) through Gαs to adenylyl cyclase to increase cyclic adenosine monophosphate (cAMP) production such that it leads to stimulation of glycogen breakdown and inhibition of glycogen synthesis, resulting in glucose production. In the eye, light stimulates the GPCR rhodopsin, which activates the G protein transducin, to stimulate the activity of cyclic guanosine monophosphate (cGMP) phosphodiesterase (PDE). This results in decreased cGMP levels and changes in the activity of the cyclic nucleotide-gated Na2+ channels, thereby converting photons into electrical impulses and transmitting information to the visual cortex. These cascades of events allow for processing of the initial signal, including amplification.