FGFR1 and X-linked hypophosphatemia: While numerous studies in both humans and mice have demonstrated a role for increased FGFR1 in articular cartilage destruction15, and conditional knockout of FGFR1 in knee cartilage reduced articular cartilage degeneration in mice16, there are no studies of the use of BGJ398 to modulate the OA phenotype in XLH subjects or Hyp mice of any age.