SOAT1 and glioblastoma: Moreover, KEGG and Reactome pathway enrichment analyses further supported that upregulated genes in the high-risk GBM formed functional networks modulating three key categories: (i) immunomodulatory pathways (e.g., JAK-STAT, chemokine and TNF signalling pathway), (ii) oncogenic signalling pathways (e.g., oestrogen, Rap1, Ras signalling pathways) and (iii) cell–matrix interactions-related processes (e.g., ECM-receptor interaction, cell surface, laminin interactions, focal adhesion, regulation of actin cytoskeleton, degradation of ECM) (Table 5; Table S12, Supplementary File S1).