Therefore, in theory at least, to minimize any potential endogenous catecholamine‐driven cancer growth or metastasis, logically, the ideal molecular pharmacological properties for an anti‐cancer β‐blocker would be (1) high β2‐AR affinity (β1‐AR and β3‐AR antagonism may be helpful in some cancers), (2) long duration of β2‐AR binding (to fully occupy all β2‐AR all of the time and prevent any adrenaline/noradrenaline‐driven cancer growth) and (3) no partial agonism. Here, ADRB3 is linked to cancer.