E2F1 and glioblastoma: The administration of delta-9-tetrahydrocannabinol (Δ9-THC) to GBM cell lines results in a significant decrease in cell viability via a mechanism that appears to elicit G1 arrest due to downregulation of E2F1, cyclin A. Δ9-THC, and cannabidiol acted synergistically to inhibit cell proliferation on the U251 and SF126 glioblastoma cell lines as an essential mediator of cannabinoid antitumoral action [216,217].