While homozygous Hhip−/− mice die shortly after birth due to defects in lung branching morphogenesis, Hhip+/− heterozygotes are viable, have normal lung development, and exhibit an approximately 33% reduction in the expression of Hhip, a level comparable to that observed in human COPD lung tissue samples harboring HHIP GWAS risk variants3. This evidence concerns the gene HHIP and chronic obstructive pulmonary disease.