The objective of this study was threefold: first, determining whether tumor β-ARs are functioning, that is, whether their stimulation causes an increase in cAMP levels; second, determining whether clonidine, the prototypical α2-AR agonist acting on all three α2-AR subtypes, affects B16F10 cell proliferation; third, assessing whether β-AR stimulation by the catecholamine isoproterenol modulates the antiproliferative action of clonidine on B16F10 cells and, if so, evaluating to what extent each β-AR subtype contributes to regulating the proliferative activity of B16F10 cells. This evidence concerns the gene ADRB2 and neoplasm.