Thus, for example, a reduction in AEA or 2-AG levels in the tumour due to over-expression of FAAH or MAGL would be expected to be deleterious by removing an antiproliferative substrate tone mediated by the ERK pathway17,33, whereas an increased synthesis of these endocannabinoids could increase tumour cell proliferation in tumours with high CB1 receptor expression by opening up survival pathways26. This evidence concerns the gene MGLL and neoplasm.