Given the increasingly frequent suggestion that AHR modulators (inhibitors or agonists) represent a new class of targeted cancer therapeutics [6,34,35,36,37,38,39,40], it is critical that additional studies be performed to determine, with a given set of readouts, tumor types and experimental models, if both AHR inhibition and hyper-activation generate similar or, paradoxically, opposite outcomes. Here, AHR is linked to neoplasm.