Although some molecular and cellular differences have been identified between mouse and human lungs (reviewed in [46]), the F0 mice generated by CRISPR/Cas9-mediated Fgf10 gene editing can become a model animal to study the pathophysiology of human pulmonary hypoplasia and related chronic lung diseases that may be rooted in the developmental stage as recently postulated [47]). This evidence concerns the gene FGF10 and chronic lung disease.