For instance, in chronic myeloid leukemia cells the BCR/ABL oncogene determines the constitutive phosphorylation of PERK and eIF2α that prevent the ER stress-dependent apoptosis in response to imatinib, as demonstrated by the re-sensitization to the drug when PERK/eIF2α activity is prevented [161]. The gene discussed is EIF2A; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.