Nevertheless, the time-course drug treatment experiments on the parental MCF-7 and drug resistant MCF-7EpiR and MCF-7TaxR breast cancer cells lent support to the idea that GCN2 can potentially cooperate with PERK to repress FOXO3 activity via JNK and AKT to modulate drug response and compensate for PERK inactivation. This evidence concerns the gene AKT1 and breast carcinoma.