CNR2 and acute promyelocytic leukemia: This effect was inhibitedby CB1 antagonism and pertussis toxin, again pointing to ERK signalingin these cells via CB1 receptors coupled to Gi/o proteins.Similarly, selective CB2 antagonism and pertussis toxin blocked 2-EG-inducedERK signaling in human promyelocytic leukemia HL-60 cells, which expressfunctional CB2 but not CB1 receptors.