Both processes arephysiologically essential: loss-of-function mutations in FAM20C cause increased bloodconcentrations of intact FGF23 and hypophosphatemic rickets (Wang et al. 2012), whereas loss-of-function mutationsin GalNT3 result in an FGF23 deficiency-like phenotype in mice and men(Topaz et al. 2004; Kato et al. 2006; Ichikawa et al. 2009). This evidence concerns the gene FGF23 and hyperinsulinemic hypoglycemia, familial, 4.