Numerous mechanisms by which gliomas induce the hyperexcitability of glutamatergic neurons have been described, including local secretion of glutamate via the system xC glutamate-cysteine exchanger(18, 29) secretion of synaptogenic factors such as glypican-3(19, 30) and thrombospondin-1(17), and dropout of inhibitory neurons in the local tumor microenvironment of glioblastoma, the mechanisms through which gliomas alter serotonergic neuronal activity – particularly at a distance – remain to be elucidated. The gene discussed is THBS1; the disease is central nervous system cancer.