Figure 1: Schematic representation of the ECS. N-arachidonoyl-ethanolamine (AEA) is mainly produced by the activity of an N-acylphosphatidylethanolamine-specific phospholipase D (NAPE-PLD), whereas its degradation is due to a fatty acid amide hydrolase (FAAH), which releases ethanolamine (Et-NH2) and arachidonic acid (AA). 2-Arachidonoylglycerol (2-AG) is also released from membrane lipids through the activity of diacylglycerol lipase (DAGL) and can be hydrolyzed by a cytosolic monoacylglycerol lipase (MAGL) that releases glycerol and AA. The cellular uptake from the extracellular to the intracellular space is ascribed to a purported “endocannabinoid membrane transporter (EMT)” that is likely to take up both AEA and 2-AG. Both eCBs trigger several signal transduction pathways by acting at their targets, CB1, CB2, GPR55, and nuclear peroxisome proliferator-activated receptors (PPARs). AEA, but not 2-AG, binds intracellularly also Transient Receptor Potential Cation Channel type 1 (TRPV1).