The above conclusion was reinforced by experiments in C6 rat glioma cells, where the effects of ketoconazole, and for comparative purposes the prototypical endocannabinoid reuptake inhibitor AM404 upon the uptake of AEA were compared with a functional measure of intracellular accumulation, namely the production of [3H]ethanolamine from the intracellularly FAAH-catalysed hydrolysis of [3H]AEA labelled in this part of the molecule. Here, FAAH is linked to glioma.