These results reveal an important role of EMT-driven DDR2 upregulation in maintaining the growth advantage but endowing YAP/TAZ-mediated ferroptosis susceptibility in recurrent tumors, highlighting potential therapeutic strategies to eradicate recurrent breast cancer cells with mesenchymal features.168 Cystine starvation activates GCN2 to increase the phosphorylation of eIF2α and the expression of the ATF4 protein and its target gene CHAC1. This evidence concerns the gene DDR2 and breast carcinoma.