In our study we provided evidence that Fgf23 is not essentially mediating pressure-induced cardiac hypertrophy in a TAC model, using two independent approaches: i) by spironolactone-induced Fgf23 suppression in WT mice, and ii) by genetic deletion of Fgf23 in Fgf23−/−/VDRΔ/Δ mice. The gene discussed is FGF23; the disease is persistent truncus arteriosus.