Genetic EGFR alterations have been found in about 60% of glioblastoma patients, leading to uncontrolled activation of signalling pathways (MAPK, PI3K/AKT, JAK/STAT, NF-κB, AKT, and others), which in turn promote cell and tumour growth, apoptosis resistance, and angiogenesis. This evidence concerns the gene SOAT1 and glioblastoma.