This interpretation is consistent with our previous work showing that eIF2αP is important for the survival of tumor cells exposed to pharmacological inhibitors of PI3K-Akt or Bcr Abl signaling [39,40] as well as with recently published work showing that eIF2αP promotes survival of a subset of hypoxic tumors that become resistant to radiation therapy [36]. The gene discussed is AKT1; the disease is neoplasm.