Our analyses also confirmed that there were no further differences in the relative levels of chondrocyte proliferation and apoptosis within the growth plates of mice with the Matn3 V194D mutation due to the deletion of Matn1. We previously proposed that these detrimental changes in the chondrocyte phenotype are key disease mechanisms in MED caused by the Matn3 V194D mutation (21, 22) and also in pseudoachondroplasia–MED caused by Comp p.T585M (28) and Comp p.D469del (33) mutations. This evidence concerns the gene MATN1 and pseudoachondroplasia.