Treatment of cells with 2DG triggers the accumulation of intracellular 2DG6P. This activates stress-signaling pathways such as cell-wall integrity signaling (CWI) or the unfolded protein response (UPR), converging onto DOG2 expression (1) [20]. On the other hand, 2DG6P elicits a fast PP1 activation (2) which causes AMPK inhibition and, either directly or indirectly, Rod1 dephosphorylation. By the time Dog2 is induced and begins to dephosphorylate 2DG6P (3), Rod1 has already triggered the endocytosis of many plasma membrane proteins (4), including that of low affinity glucose transporters. This may prevent 2DG exit and detoxification but also affect cell survival by reducing glucose import (5).