PERK/eIF2α/ATF4 has also been implicated in increased proliferation and survival of hypoxic cancer cells.41,42 Tumors derived from PERK−/− mouse embryonic fibroblasts have limited ability to stimulate angiogenesis.43 Supporting this notion, Bi et al. demonstrated a functional link between the activation of the PERK/eIF2α/ATF4 pathway and the upregulation of vascular endothelial growth factor-A (VEGF-A) transcription.41 The gene discussed is EIF2AK3; the disease is cancer.