However, the deletion of CB1 resulted in more rapid cancer growth in a genetic mouse model of CRC [47] in APCMin/+ mice, while treatment of Cnr+/+/APCMin/+ mice with CB1 agonist R-1 methanandamide resulted in tumor growth inhibition through downregulation of anti-apoptotic factor: survivin. The gene discussed is CNR1; the disease is neoplasm.