The mechanism for this apparent altered behavior of cancer cells depending on the density of MOR expression may be multifactorial and involve cross activation of genes which are pro-metastatic including the proto-oncogene (Src), signal transducer and activator of transcription 3, neuroepithelial cell-transforming gene 1 protein [22] and the serine/threonine-specific protein kinase (Akt) [16], all of which are expressed in tumors with high metastatic potential. This evidence concerns the gene STAT3 and cancer.