β-endorphin (bEP) neuron activation prevents the growth and metastasis of mammary tumor cells by altering autonomic nervous system activities that enhance innate immune functions. Sarkar and colleagues identified the mechanism by which bEP cell transplantation into the brain prevents mammary carcinogenesis by showing that the transplants' antimetastatic effect, along with stimulation of cytotoxic function of immune cells and production of anti-inflammatory cytokines, is reversed by the treatment with an opiate antagonist, naloxone (NAL), to block bEP, the β-receptor agonist metaproterenol (MET) to activate sympathetic neurotransmission, or the nicotine acetylcholine receptor antagonist methyllycaconitine (MLA) to prevent parasympathetic neurotransmission. For details, see the article by Sarkar and colleagues on page 6282 of this issue.