In addition to blocking FAAH, inhibition of MAGL as a potential antitumour strategy has also attracted the attention of scientists in recent years, as it not only induces anticarcinogenic effects by activating cannabinoid receptors via 2-AG, but also reduces a number of tumour-promoting fatty acids (Figure 1) that would contribute to tumour growth via various mechanisms when MAGL is overactive (for review see [14,102]). The gene discussed is MGLL; the disease is neoplasm.