The hypothesis that the β-adrenergic system - and more specifically β2-ARs - was involved in the coupling mechanisms between hypoxia and vascularization originated from the serendipitous clinical observation in humans that treatment with propranolol, a non-selective β1/β2-AR blocker, led to regression of infantile hemangiomas (IH) (32), the most common benign vascular proliferative lesion in infants, typically triggered by preexisting ischemic and hypoxic conditions (33). The gene discussed is ADRB2; the disease is capillary hemangioma.