Moreover, in the setting of brain tumors, glutamatergic synaptic input to glioma cells drives malignant glioma progression [56], whereas increased neuronal excitability resulting from light exposure leads to the secretion of ADAM10 that cleaves membrane-bound neuroligin-3 on oligodendrocyte precursors to induce Nf1 optic glioma initiation and growth [42]. Here, NLGN3 is linked to brain neoplasm.