An article appearing in this issue of the British Journal of Pharmacology shows for the first time that the general anaesthetic propofol inhibits one of the enzymes catalysing endocannabinoid hydrolysis and inactivation, the fatty acid amide hydrolase, thereby enhancing the brain levels of anandamide and 2-arachidonoylglycerol in mouse brain. The authors provide evidence that this effect of propofol underlies part of the sedative effects of this compound. The importance of these findings in the light of the likely role of the endocannabinoid system in the control of sleep-wake cycles, and of the possibility of developing therapeutic drugs from substances that manipulate endocannabinoid levels, is discussed.