In summary, they compared the bone development in animal models where CNP was switched off or produced in excess with normal animals and found that those animals where CNP was over produced turned to have longer cranial bones than the normal animals, while the animals without CNP had shorter cranial bones.
Why this is important for achondroplasia?
One of the hallmarks of achondroplasia is the low development of the bones in the middle of the face, which produces the typical low nasal bridge. It is then expected that by offering CNP as a therapeutic approach to treat achondroplasia, that not only the long bones and spine will tend to recover their growth pace but also the therapy should be capable of recover the growth of bones located in the midface of affected individuals. With better developed bones in the face, one could expect that treated children would have less upper respiratory tract complications such as obstructive sleep apnea, ear and upper airway infections.
As the first CNP analogue (BMN-111) is now to enter phase II of the clinical development, it would be interesting to include indexes of cranial bone growth in clinical trial procedures, because this should be another marker of the bone response to therapy with CNP. You can learn more about drug clinical development here and more about CNP here.