Tumor microenvironments (TMEs) play a critical role in HGGs progression, and recent evidence suggests that myelin could act as a pro-differentiative niche - since tumor cell differentiation could be influenced by the selective upregulation of SOX10 - while glioma stem cells exploit Notch-Jagged1 signaling to migrate along demyelinated white matter tracts, potentially influencing both disease development and relapse mechanisms [4–13]. This evidence concerns the gene JAG1 and neoplasm.