In light of the recent discovery that COMP interacts with matrilin-1, -3, and -4[21], our finding here lends support to the hypothesis that mutations in any of these interacting proteins including matrilin, COMP, or collagen IX, result in a secretion defect, which manifests in common chondrodysplasia pathological phenotypes. This evidence concerns the gene MATN1 and chondrodysplasia.