Rapamycin is a potent immunosuppressant that affects the cellular protein translation machinery. The cellular targets of rapamycin, FRAP/RAFT1/mTor in mammals and Tor1p/Tor2p in Saccharomyces cerevisiae, are members of the PI3-kinase related family of protein kinases. Rapamycin inhibits the catalytic activity of these serine protein kinases while at the same time activating protein phosphatase 2A, events that have the effect of sharply reducing the phosphorylation and function of p70S6K and eIF-4E binding protein. Recent studies have suggested that FRAP is involved in a cell-cycle checkpoint mechanism that senses intracellular nutrient availability by sampling levels of free amino acids. Here we used DNA microarrays to investigate the effects of rapamycin exposure or amino acid deprivation on the transcriptional program of the budding yeast S. cerevisiae. We show that over a period of two hours the transcriptional response to rapamycin exposure is similar to the response following amino acid starvation in both haploid and diploid cells. The transcriptional response to rapamycin appears to be a subset of a more extensive transcriptional response induced by amino acid withdrawal. Our results suggest that Tor protein inactivation elicits most features of a nitrogen starvation response in yeast even in the presence of abundant nutrients. Our results also indicate the ease with which a genome-based approach is able to identify the intracellular pathway targeted by a small molecule drug.