The existence of programmed cell death in Saccharomyces cerevisiae has been reported for many years. Glucose induces the death of S. cerevisiae in the absence of additional nutrients within a few hours, and the absence of active potassium uptake makes cells highly sensitive to this process. S. cerevisiae cells possess two transporters, Trk1 and Trk2, which ensure a high intracellular concentration of potassium, necessary for many physiological processes. Trk1 is the major system responsible for potassium acquisition in growing and dividing cells. The contribution of Trk2 to potassium uptake in growing cells is almost negligible, but Trk2 becomes crucial for stationary cells for their survival of some stresses, e.g. anhydrobiosis. As a new finding, we show that both Trk systems contribute to the relative thermotolerance of S. cerevisiae BY4741. Our results also demonstrate that Trk2 is much more important for the cell survival of glucose-induced cell death than Trk1, and that stationary cells deficient in active potassium uptake lose their ATP stocks more rapidly than cells with functional Trk systems. This is probably due to the upregulated activity of plasma-membrane Pma1 H ⁺ -ATPase, and consequently, it is the reason why these cells die earlier than cells with functional active potassium uptake.