Whilst it is tempting to conclude that CB1/2 activation is of benefit in the treatment of cancer-induced pain, we propose the followings: First, the analgesic effects of the CB1/2-non-selective endocannabinoids and synthetic CP55,940 and WIN55,212-2 should be validated in genetically modified animal models lacking CB1, CB2 and most importantly both receptors. Here, CNR2 is linked to cancer.