Mechanistically, tumor cell differentiation is driven by selective white matter upregulation of SOX10, a master regulator of normal oligodendrogenesis. SOX10 overexpression or treatment with myelination-promoting agents that upregulate endogenous SOX10, mimic this response, leading to niche-independent pre-oligodendrocyte differentiation and tumor suppression in vivo. Thus, glioblastoma recapitulates an injury response, and exploiting this latent program may offer treatment opportunities for a subset of patients ¹⁾.