Additionally, the same project described three major pathways that are usually involved in GBM pathogenesis—the tumour protein p53 (P53) pathway, the receptor tyrosine kinase/Ras/phosphoinositide 3-kinase (PI3K) signalling pathway and the retinoblastoma (RB) pathway—whose mutations lead to the excessive proliferation of tumour cells by augmenting cell lifespan via apoptosis inhibition and increasing the proliferation rate [24]. Here, TP53 is linked to glioblastoma.