The Ras/cAMP pathway in the yeast S. cerevisiae couples the cell cycle of this unicellular organism to the availability of nutrients. Glucose derepressed S. cerevisiae cells respond to glucose addition by an intracellular rise in cAMP. In the prevailing model, yeast Ras plays a similar role to that of heterotrimeric G-proteins coupled to cell surface receptors. A crucial element of this model is that the exchanger, Cdc25 is activated by glucose. Such activation would result in a glucose-dependent rise in GTP-bound Ras concentration. We here show, in contrast to this view, that Cdc25 cannot be the receiver of the glucose signal. We suggest that the Ras-GTP/cyclase complex is the molecular element directly receiving the signal while Cdc25-dependent exchange constitutes a prerequisite for complex formation.