Recent studies of target of rapamycin (TOR) in fission yeast revealed that in this organism, like in budding yeast and human cells, the TORC1 complex containing TOR together with a raptor-like protein, plays a central role in regulating growth, while inhibiting starvation responses. Disruption of TORC1 in fission yeast results in a phenotype very similar to that of wild-type cells starved for nitrogen, suggesting that TORC1 may regulate growth in response to nitrogen availability. The TORC2 complex in fission yeast contains TOR together with a rictor-like protein. In fission yeast, this complex is not essential under normal growth conditions but is required for survival under stress and for starvation responses. More recent studies demonstrate that TORC2 in fission yeast also has a profound role in gene silencing, telomere length maintenance and DNA damage response. Most interestingly, rapamycin does not inhibit the essential role of TORC1 or most of the cellular functions of TORC2. Yet, accumulation of data suggests that rapamycin can inhibit either TORC1- or TORC2-dependent functions under certain nutritional growth conditions and/or in the presence of loss-of-function mutations in TORC1 or its regulators. Understanding the determinants that render cells sensitive to rapamycin is critical for understanding the mode of action of rapamycin and may also extend our understanding of potential interactions between TOR containing complexes.