Endoplasmic Reticulum (ER) stress is the hallmark of many diseases and specifically, cancer cell growth and metastasis. We identified a novel translational control mechanism that operates during chronic ER stress which had not been recognized before (Mol Cell 2017). We have recently contributed with novel insights in the metabolic reprogramming of cells by the post-translational modification of redox-sensitive cysteine residues during chronic ER stress (eLife 2015and MCP, 2020). Both of these findings lead to the discovery of unique stress adaptation mechanisms in cancer cells to stress, that can be targeted for therapeutics. Our current focus is breast cancer and glioblastoma stem cells.