BACKGROUND: Rac 1 is a small G-protein which can activate NF-kappaB. Pentadecapeptide BPC 157 decreases transcription of Vcam1 in NF-kappaB signalling pathway like some NF-kappaB inhibitors and supresses ERK induction of Vcam1 through NF-kappaB activation. Pentadecapeptide BPC 157 can be Rac1 activator or inhibitor, and that could depend on phosphorylation site of FAK/Paxillin pathway. METHODS: Review of pentadecapeptide BPC 157 and Rac1 inhibitor effects on tumour growth, ischemia-reperfusion injuries, ulcerative colitis, viral infections, multiple sclerosis, depression and healing, as well as comparison with the effects of NF-kappaB inhibitors. RESULTS: Pentadecapeptide BPC 157 could be a novel NF-kappaB inhibitor. While most of the research on Rac1 inhibitors is done in models of tumour growth inhibition where Rac1 overexpression is found, the research on BPC 157 is focused on inflammation diseases and healing. The NF-kappaB transcription factor is a link between inflammation and cancer, so it is possible that NF-kappaB pathway is a connection between pentadecapeptide BPC 157 and Rac1 inhibitors. Pentadecapeptide BPC 157 and NF-kappaB inhibitors have positive result in all of the models reviewed, while Rac1 inhibition is not affective in models of healing and depression. CONCLUSION: It is possible that the NF-kappaB transcription factor is a cause of the similirality between BPC 157 and Rac1 inhibitors in some of the models. Other signalling pathways , like ERK and CREB must be considered, as well as the fact the effect of BPC 157 and Rac1 inhibitors on NF-kappaB could be cell specific.