Painful stimuli cause the release of endogenous opioids, activating MOR and causing analgesic responses. In this way MOR is responsible for mitigating the sensation of pain in the absence of opioid medication. There are a number of different classes of pain, which include nociceptive, neuropathic, inflammatory and pathological pain [11]. Various forms of painful stimuli result in different biochemical and physiological responses and it is, therefore, likely that there are differences in the effects of genetic variations on the thresholds and tolerance levels for different types of pain. Due to the involvement of MOR in analgesia, Fillingim et al. assessed the effects of the A118G polymorphism on pain from three different sources: pressure, heat, and ischemia [12]. Individuals carrying the G allele were found to have higher thresholds for pressure pain, while no differences were observed in ischemic pain [12]. For thermal pain, men with the G allele reported lower pain ratings, while women reported more pain [12]. Another study found the minor allele of the intronic variant rs9479757 to also be associated with a higher pressure pain threshold [13].