MATN3 and multiple epiphyseal dysplasia: We have deleted the IRE1/XBP1 pathway activity in the chondrocytes of a mouse model of multiple epiphyseal dysplasia (MED), expressing misfolding matrilin-3 predominantly in proliferating chondrocytes, and in metaphyseal chondrodysplasia type Schmid (MCDS), resulting from mutations in type X collagen, expressed by the hypertrophic chondrocytes.