MATN3 and multiple epiphyseal dysplasia: In conclusion, this study has discovered that the aggregation of mutant matrilin-3 is a key disease trigger in this form of MED, and that the prevention of this protein accretion, by either enhancing the folding with corrector-molecules (54,55) or preventing non-native disulphide bond formation by blocking the unpaired cysteine residues (56), offers novel therapeutic targets for further validation.