Here, to obtain the proof-of-principle that also in the human kidney the pharmacological agonism of the β3-AR promotes the trafficking of AQP2 and NKCC2, we analyzed the 24 h urine of a cohort of patients with overactive bladder syndrome (OAB) [11,12,13], with apparent normal renal function, before and during chronic treatment (up to 12 weeks) with the human β3-AR agonist mirabegron [14], given to relief symptoms of the disease. The gene discussed is SLC12A1; the disease is Urinary urgency.