The biochemical hallmarks of XLH include hypophosphatemia, elevated alkaline phosphatase (ALP) indicating increased osteoblast activity due to rickets/osteomalacia, decreased tubular maximum reabsorption of phosphate per glomerular filtration rate (TmP/GFR) indicating renal phosphate wasting, and non-suppressed levels of intact FGF23 despite hypophosphatemia suggesting FGF23-mediated renal phosphate wasting. The gene discussed is FGF23; the disease is X-linked hypophosphatemia.