The functional modulation of KCC2 activity has been observed both in physiological and pathological models, such as prolonged post-synaptic spiking,25 brain-derived neurotrophic factor (BDNF) stimulation26 and oxygen glucose deprivation.18 Our data suggest that the mechanism responsible for glioma-induced KCC2 inhibition relies on Zn2+-mediated Src/TrkB activation. The gene discussed is NTRK2; the disease is central nervous system cancer.