Hydrostatic pressure leads to activation of the TOR complex 1 (TORC1) nutrient signalling pathway, which controls protein synthesis and cell growth. In Saccharomyces cerevisiae, mutants of the Ego complex (EGOC) proteins Ego1 and Ego3 and the GTPases Gtr1 and Gtr2, all of which are involved in TORC1 signalling, have been shown to display growth defects under pressure, but the role of TORC1 in this situation is still poorly understood. Now, Fumiyoshi Abe and colleagues (Uemura et al., 2020) show that TORC1 stimulation is important to avoid amino acid accumulation under high pressure. By subjecting S. cerevisiae cells to forces of 25 MPa (∼250 kg/cm2), the authors observe that EGOC components and Pib2, a recently identified TORC1 regulator, are necessary for Tor1 localisation at the vacuolar membrane. This leads to TORC1 activation upon pressure and phosphorylation of its target Sch9, which is abolished in ego1Δ, ego3Δ and pib2Δ mutants, impairing growth. Notably, ego1Δ, gtr1Δ, tor1Δ and pib2Δ mutants show increased levels of glutamine and alanine under pressure, but not because of effects on the translation machinery. Based on these data and previous in vitro studies, the authors hypothesise that pressure-induced glutamine accumulation activates EGOC–TORC1 through Pib2 to downregulate glutamine levels. This study therefore uncovers the role of TORC1 in yeast tolerance to high pressure and provides new insights into the metabolic adaptations that occur under mechanical stress.