Regulation of iron or phosphate homeostasis by C-terminal vs full-length FGF23. Inflammation, iron deficiency, and phosphate-related stimuli activate FGF23 transcription in osteocytes. Newly translated FGF23 protein is either glycosylated by GALNT3 and secreted into circulation to regulate phosphate homeostasis or phosphorylated by Fam20C and cleaved by furin. Courbon et al demonstrate that inflammation also increases expression of Fam20C and Furin and decreases GALNT3 expression. C-terminal FGF23 fragments are secreted by osteocytes and travel to the liver to antagonize BMP-mediated increases in hepcidin production. Presumably, N-terminal FGF23 fragments are also secreted, but their potential biological functions are currently unknown. Professional illustration by Somersault18:24.