This inhibitory effect on cancer progression by MAGL inhibition appears to be due to a dual-mode effect in prostate cancer cells involving both activation of CB1 receptor by increasing 2-AG levels and reduction of protumorigenic free fatty acids resulting from MAGL activity [30], whereas for the anti-invasive effect on lung cancer cells, only CB1 receptor involvement has been demonstrated [32]. This evidence concerns the gene MGLL and lung carcinoma.