In addition to its histological complexity, GB pathogenesis involves extensive molecular heterogeneity, including alterations in key oncogenic pathways such as receptor tyrosine kinase (RTK), p53, and retinoblastoma (RB), as well as an immunosuppressive and pro-angiogenic tumor microenvironment (TME) driven by hypoxia-induced vascular endothelial growth factor (VEGF) expression and the recruitment of tumor-associated macrophages (TAMs). Here, TP53 is linked to neoplasm.