This effect of ibuprofen was outlined in experimental designs for acute pain and also for neuropathic pain. Guindon T, et al. 2006 figured ibuprofen potentiated the exogenous cannabinoids. Flurbiprofen, an ibuprofen derivative, intrathechally administrated proven an analgesic effect mediated by the endocannabinoid potent c-Met inhibitor system, as derive from Ates M, et al. 2003, Seidel E, et al. 2003 and Bishay R, et al. 2010. Some nonselective COX inhibitors, such as ketoprofen, sulindac and naproxen were examined by Anikwue Dtc, et al. 2002, who showed why these substances did not act directly or indirectly on CB1 or CB2 receptors. On another hand, discomfort proved to potentiate the effect of CB2 receptor agonist, a CB1 and HU-210. After Naidu PS, et al. 2009 diclofenac acted synergistically with URB 597. Ketorolac, a selective inhibitor of COX1, had additive effects in association with WIN 55212 2, a nonselective cannabinoid agonist. Nevertheless, other authors, like Anikwue Dhge, et al. 2002, proved that ketorolac did not work directly or indirectly on cannabinoid receptors. The selective Gene expression COX2 agonists: NS 398, respectively rofecoxib, potentiated the action of cannabinoid agonists in acute pain models or in neurophatic pain models. Celecoxib might not have a cannabinoid result in the Dhge, et al. 2002 research, while nimesulide showed an impact on receptors without inference on anandamide or 2 AG levels. From each of the ingredients contained in the NSAIDs group, acetaminophen was studied one of the most regarding its interferences with the system mainly due to contradictory results. H gest tt ED, et al. 2005 showed that acetaminophen could possibly be transformed in AM 404 within the central nervous system by FAAH. This metabolite is an agonist on COX2 inhibitor, a COX1 and TRPV1 receptors and inhibits the reuptake of anandamide, having an analgesic effect. There are several studies using acute pain models recognized on animals performed by Ottani A, et al. 2006 and Mallet H, et al. 2008 and other studies done on neuropathic pain models performed by Dani M, et al. Hama and 2007 AT and Sagen deubiquitinating enzyme inhibitors T. 2010 which sustain the existence of cannabinoid effects for acetaminophen. Other studies had other effects. Sagen 2010 and hama AT and Costescu M, et al 2010 studied the association between acetaminophen and gabapentin, morphine or ibuprofen. They concluded that CB receptor blockers can antagonize the analgesic effects of these associations. Results 1. A clear villain, chemical or synergic effect of NSAIDs cannabinoid organizations was not yet confirmed. One of the causes for the range of experimental results presented could be due to pharmacokinetic elements, according to the route of administration and the measure. Some NSAIDs have additional influences to the cannabinoid system both by inhibiting FAAH, or by inhibiting a feasible intracellular transporter of endocannabinoids.