However, expression levels of EAAT2 are vastly reduced in gliomas, which combined with increased efflux via the glutamate/cystine antiporter (xCT, SLC7A11) leads to elevated glutamate levels surrounding the glioma that induce cell death and allow further growth of the tumor (Takano et al., 2001; Robert and Sontheimer, 2014). This evidence concerns the gene SLC1A2 and neoplasm.