We then explored whether we could selectively inhibit TRPV4 mechanotransduction bytargeting expression of the CD98 HH domain as a therapeutic for pulmonary vascular disease.Using the optimized AAV vectors, we investigated whether the delivery of CD98 HH could beused to rescue the compromised pulmonary barrier function in a human Lung Alveolus Chip,which has been previously shown to model multiple physiological and pathophysiologicalfeatures of the human lungs, including pulmonary edema.13,41. This evidence concerns the gene TRPV4 and pulmonary edema.