This seems paradoxical at first glance, but HPP patients, who display increased concentrations of PLP within their blood serum, exhibit a lack of the same molecule within the brain, as only the dephosphorylated form (PL), which is provided by TNAP, is able to cross the blood–brain barrier (BBB), and is subsequently re-phosphorylated [75]. The gene discussed is ALPL; the disease is hypophosphatasia.