Morphine may be the major drug of choice in the critical stage of cancer pain. Individuals suffering from bone cancer pain usually involve significantly larger doses of morphine as in comparison to people who have inflammatory pain. The doses of morphine required to order Crizotinib block bone cancer pain in mouse are five times that required to block top inflammatory pain behaviors. Sasamura et al. Noted that subcutaneous morphine, at the dose of 5 mg/kg, prevents melanoma induced heat hyperalgesia. In our research, this dose of morphine inhibited melanoma induced mechanical allodynia however not heat hyperalgesia when examined after 3 hours. Repeated injections of morphine caused a rapid development of analgesic tolerance in the second time, which can be faster than that observed in another skin cancer model. Morphine caused threshold results in increased drug use and incidence of negative effects, such as for example sleep, constipation, itching, nausea, sickness Metastatic carcinoma and respiratory depression. Morphine also causes rapid tolerance in neuropathic pain models. The rapid development of morphine tolerance in cancer bearing rats further supports a neuropathic involvement in this cancer pain model. Our data claim that morphine only has limited role in controlling the pain symptoms in intense skin cancer states. Morphine was demonstrated to control cyst growth in a cancer model. This anti tumor effect of morphine could be from the analgesic effect of morphine, because cancer pain results in psychological stress that will enhance tumor growth and suppress immune features. On the other hand, morphine at high doses enhances tumor growth because of the suppression of defense mechanisms. In this study, morphine had no effect on the growth of melanoma, which can be hedgehog antagonist correlated with minimal analgesic effect of morphine in the melanoma model. We have characterized a skin cancer pain type induced by intraplantar inoculation of cancer cells in to a hindpaw. This type is seen as an sturdy tumefaction development and rapid development of heat and mechanical hypersensitivity and displays marked peripheral neuropathy. Given the lower incidence of pain in cancer patients, this product might not be very clinically relevant compared to other models, for example bone cancer pain models. However, this model is quite easy to study mechanisms of cyst growth and cancer pain and to try new treatment. Future studies will be required to try the position of the JNK pathway in other cancer pain types. Our data have shown that repeated administration of the peptide inhibitor of JNK, D JNKI 1, not just attenuates melanoma induced mechanical allodynia but also suppresses tumor development both in vitro and in vivo. In contrast, repeated administration of morphine shows no effect on tumor growth and provides quick analgesic tolerance. It is worthwhile to examine JNK with its member of the family p38. Both MAPKs are pronociceptive. Spinal administration of p38 inhibitors was demonstrated to attenuate neuropathic pain and inflammatory pain in different designs.