GADD34-mediated dephosphorylation of eIF2α-P during mild hyperosmotic stress promotes adaptation. The adaptation program during hyperosmotic stress involves TonEBP-mediated transcriptional control of genes coding for transporters of compatible osmolytes, including the neutral amino acid transporter SNAT2. In contrast, induction of eIF2α phosphorylation promotes apoptosis. The model suggests that the MAP kinases signaling promote survival via induction of GADD34, which dephosphorylates eIF2α-P and, therefore, inhibits apoptosis. The proapoptotic signaling of eIF2α-P also contributes to the inhibition of the prosurvival SNAT2-mediated increased amino acid uptake.