GRIN2A and neoplasm: 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.