Pharmacological activation of CB1Rs upon systemic administration of cannabinoid agonists triggers tumour-cell apoptosis in numerous mouse models of cancer, especially glioblastoma, the most common form of brain cancer [62,63], but to which extent this event relies, at least in part, on CB1R molecules located on tumour-microenvironment-forming cells (such as neurons in MBMs) remains largely unknown. The gene discussed is CNR1; the disease is glioblastoma.