Although we could not demonstrate any phenotypic differences between Matn1+/+Matn3m/m and Matn1−/−Matn3m/m mice, we cannot exclude the possibility that the retention of these hetero-oligomers, along with the more prevalent matrilin 3 homo-oligomers, contributes to the etiology of MED. Here, MATN1 is linked to multiple epiphyseal dysplasia.