Disruption of the ECM components necessary for the template formation and mineralization of cartilage, bone, dentin, and cementum have been reported in the mouse model for XLH (PhexHyp mouse), suggesting that loss of PHEX function and/or hypophosphatemia may disrupt ECM deposition (Liang et al., 2011; Salmon et al., 2013, 2014; Coyac et al., 2017, 2018). This evidence concerns the gene PHEX and X-linked hypophosphatemia.