NLGN3 can also stimulate several oncogenic pathways, such as activation of focal adhesion kinase (FAK), and upregulation of several synapse‐related genes in gliomas cells.19, 20 The neuronligin‐3 is cleaved from both neurons and oligodendrocyte precursor cells (OPCs) via ADAM10 sheddase, and the ADAM10 inhibitors can prevent the release of NLGN3.20 This evidence concerns the gene ADAM10 and central nervous system cancer.