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The protein ovocleidin\u2010116 is one of these proteins with an ancestry stretching back to the Triassic. Ovocleidin\u2010116 is an avian homolog of Matrix Extracellular Phosphoglycoprotein (MEPE) and belongs to a group of proteins called Small Integrin\u2010Binding Ligand Interacting Glycoproteins (SIBLINGs). The genes for these NCPs are all clustered on chromosome 5q in mice and chromosome 4q in humans. A unifying feature of the SIBLING proteins is an Acidic Serine Aspartate\u2010Rich MEPE (ASARM)\u2010associated motif. The ASARM motif and the released ASARM peptide play roles in mineralization, bone turnover, mechanotransduction, phosphate regulation and energy metabolism. ASARM peptides and motifs are physiological substrates for phosphate\u2010regulating gene with homologies to endopeptidases on the X chromosome (PHEX), a Zn metalloendopeptidase. Defects in PHEX are responsible for X\u2010linked hypophosphatemic rickets. PHEX interacts with another ASARM motif containing SIBLING protein, Dentin Matrix Protein\u20101 (DMP1). DMP1 mutations cause bone\u2010renal defects that are identical with the defects caused by loss of PHEX function. This results in autosomal recessive hypophosphatemic rickets (ARHR). In both X\u2010linked hypophosphatemic rickets and ARHR, increased fibroblast growth factor 23 (FGF23) expression occurs, and activating mutations in FGF23 cause autosomal dominant hypophosphatemic rickets (ADHR). ASARM peptide administration <jats:italic>in vitro<\/jats:italic> and <jats:italic>in vivo<\/jats:italic> also induces increased FGF23 expression. This review will discuss the evidence for a new integrative pathway involved in bone formation, bone\u2010renal mineralization, renal phosphate homeostasis and energy metabolism in disease and health. 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