A recent study showed that hyper-IL-6 (HIL-6) activates the FGF-23 promoter by STAT3 phosphorylation and increases circulating FGF-23 in both AKI and CKD.54 Activation of FGF receptor 1 (FGFR1) further increases FGF-23 synthesis in folic acid-induced AKI.55 Moreover, decreased FGF-23 clearance in AKI also contributes to high circulating levels of FGF-23.11 However, whether FGF-23 plays a functional role in mediating AKI is an important topic and remains to be explored. The gene discussed is STAT3; the disease is chronic kidney disease.