This subsequently triggers NRF2-mediated antioxidant downstream effects, augmented cystine uptake, and glutathione metabolism, ultimately promoting drug resistance and quiescent transition in breast cancer cells.154 Conversely, excessive mechanical forces (450 Pa) in the ECM have been shown to induce dormancy in stem-like breast cancer cells via the DDR2/STAT1/p27 signaling cascade, with mechanical force removal potentially leading to dormancy reactivation.153. This evidence concerns the gene STAT1 and breast cancer.