Since the 1970s, it has been known that cannabis can inhibit the growth of certain types of cancer. Many cancers express components of the ECS with some cancer types overexpressing certain endocannabinoids or receptors. The ECS is known to participate in a great number of signaling pathways that control normal cell growth as well as tumor growth through a variety of different mechanisms such as induction of autophagy or apoptosis. The ECS is able to do this via a large variety of intracellular signaling pathways including ERK1/2 pathways, AKT pathway, ceramide, ASK1 and p38MAPK/JNK pathways, p8 signaling pathways, and inhibition of the mTORC1 pathway, tribbles homolog 3 (TRB3), Akt/mToRC1 axis and AMPK, JNK/p38 MAPK, Bio, p53, p42/44, and ASK1. TRPV, GPR55, and PPAR gamma have also been implicated in the regulation of cell survival. The ECS is also involved in other potential antineoplastic processes such as cell cycle arrest, prevention of metastasis, and antiangiogenesis. Signals implicated in cell cycle arrest include cdc-2, Chk1, Cdc25A, Cdk2, and bFGF. In some cancer types, antiangiogenesis effects were mediated by ECS downregulation of COX-2 and VEGF. AEA-treated cancer cells decreased phosphorylation of two tyrosine kinases: FAK and Src via CB1 activation, which the authors of the study thought was the mechanism behind the decreased adhesion and migration. Excess cannabinoids maybe detrimental in some forms of cancer as well as presumably by downregulating the immune response to the cancer.