Mutations that seem functionally similar in other individuals produce lipodystrophy, not pulmonary hypertension, which makes it seem likely that the reason that we did not see pulmonary hypertension in these mice is that they lacked the underlying polymorphisms associated with disease in the patients, although it could be due to differences between human and mouse anatomy or Cav1 function. Here, CAV1 is linked to pulmonary arterial hypertension.