SLC6A8 and neoplasm: Here, we reveal a novel molecular mechanism of tumor cells maintaining appropriate mitochondrial ROS levels under hypoxia, that is, hypoxia activated p65/NF-κB signaling induces expression of SLC6A8 and creatine accumulation to upregulate antioxidant capacity in TNBC cells, which provides a new mechanistic insight into the control of oxidative stress in hypoxic tumor cells.