In the late 1950s the Swiss pediatric endocrinologist Andrea Prader was the first to identify a case of acquired hypophosphatemia caused by a ricketogenic substance [FGF23].(1, 2, 3) It would take more than 40 years to clone this humoral factor, or phosphatonin, causing renal phosphate wasting.(4) Studies of autosomal dominant hypophosphatemic rickets led to identifying FGF23 as the most common phosphatonin, crucial in both physiologic phosphate regulation and the driver of phosphate wasting in multiple diseases.(4, 5, 6). Here, FGF23 is linked to autosomal dominant hypophosphatemic rickets.