The contrasting consequences of triggering particular ARs, on the survival, proliferation or migration and invasiveness of tumor cells most probably occur due to the heterogeneity between cells and/or experimental settings employed to assess them. For instance, two different cancer cell lines of distinct tissue origin could have profoundly diverse AR expression profiles as well as different ability to transmit/terminate signaling initiated by these receptors. Moreover, they might have different capacity to produce adenosine, which once released into the medium can trigger ARs in an autocrine fashion. Finally, different concentrations used between experiments, as well as limited specificity of the AR agonists/antagonists, probably constitute additional factors contributing to the observed discrepancies.