Recently, PDGF-BB was shown to increase intracellular Pi uptake by regulating the membrane migration of PiT-1 by activating protein kinase B (AKT) signaling in human neuroblastoma SH-SY5Y cells [104], indicating that increased PDGF-B/PDGFR-β signaling may contribute to intracellular Pi uptake in the central nervous system (CNS), but it is unclear whether decreased PDGF-B/PDGFR-β signaling in the CNS has an influence similar to SLC20A2 mutations on normal intracellular Pi uptake and leads to extracellular Pi accumulation. This evidence concerns the gene PDGFRB and neuroblastoma.