One proposal is that the presence of tumor provides a source of an unknown self-antigen, leading to expansion of T and B leukocyte cells and tumor-specific antibodies, ultimately resulting in cross-reactivity with NMDARs [40]; because there is a strong correlation between excitotoxic cell death, mental dysfunction, and increased calcium influx [41, 42], it has been proposed that circulating antibodies and cytokines cross the blood brain barrier, modulate NR2A and NR2B subunits in the hippocampus and neocortex of brain, and increase calcium conductance. This evidence concerns the gene GRIN2B and neoplasm.