Collectively, their data suggested that cannabinoids, through the activation of CB1 and CB2 receptors as well as TRPV1, increased the TIMP-1 release from lung cancer cells via activation and subsequent induction of intercellular adhesion molecule 1 (ICAM-1) expression, thereby altering the cancer cell microenvironment and suppressing the angiogenic potential of endothelial cells [70]. This evidence concerns the gene ICAM1 and lung carcinoma.