With respect to the functional implication of endocannabinoids in tumor progression, as early as two decades ago AEA was shown to confer a concentration-dependent inhibitory effect (maximal inhibition at 10 μM) on the proliferation of nerve growth factor-activated breast cancer cells via activation of CB1 receptors and downstream inhibition of endogenous prolactin action (De Petrocellis et al., 1998). This evidence concerns the gene NGF and breast cancer.