Attenuation of the OGF-OGFr axis in cancer cells through: i) disruption of OGF-OGFr interfacing by continuous exposure to opioid antagonists (e.g., naltrexone, NTX) [14,17,19], ii) neutralization of OGF by antibodies to the peptide [14,24], or iii) a decrease in OGFr by antisense cDNA or siRNA for OGFr [24,25], stimulates cell proliferation. This evidence concerns the gene OGFR and cancer.