Ni et al. (2017) demonstrated that activated NTRK2 alleles, especially the human tumor-associated QKI-NTRK2 fusion, could function together with Ink4a/Arf loss to promote astrocytoma formation. Furthermore, a recent study found that the interaction between differentiated glioblastoma cells and stem-like tumor cells via BDNF-NTRK2-VGF paracrine signaling accelerates tumor growth (Wang et al., 2018b). This evidence concerns the gene CDKN2A and astrocytoma (excluding glioblastoma).