While normal cells preserve membrane localization of EAATs, their mislocalization in malignant cells together with up-regulation of xCT lead to aberrant handling of glutamate that induces high levels of glutamate in the extracellular space, as seen in gliomas (192) and in breast cancer, where endocrine therapy-resistant cells promote autophagy and glutamate import via EAAT2 (60, 193). This evidence concerns the gene SLC7A11 and breast carcinoma.