Fibroblast growth factor 23 (FGF23) regulates phosphate and vitamin D metabolism and induces left heart hypertrophy. The importance of FGF23 is supported by the consequences of FGF23 deficiency: FGF23-deficient mice have a significantly reduced life span and recapitulate human age-associated diseases. Moreover, FGF23 has gained attention as a potential disease biomarker due to its positive correlation with disease activity, progression, and outcome in chronic kidney disease or cardiovascular disorders. It is, however, not entirely clear whether FGF23 merely indicates disease or actively contributes to disease progression. Therefore, it is important to explore the regulation of FGF23 production, which is similarly incompletely understood. Our paper identifies fundamental insulin/IGF1-dependent PI3K/Akt/FOXO1 signaling as a key suppressor of FGF23 formation.