PNAS 115, 2788–2793 (2018)

Humans have a single gene that codes the alpha-1 antitrypsin protein; mutations that cause deficiencies can contribute to pulmonary diseases like emphysema. Mice have six, complicating efforts in the past to create genetic animal models. But those extra genes have proved no match for CRISPR.

Using the gene-editing technology to target conserved regions across the murine genes, researchers led by Chris Mueller at the University of Massachusetts Medical School managed to knock out five of those paralogs. Symptoms characteristic of emphysema can be induced in young mice with a lipopolysaccharide challenge, but will also spontaneously develop as the mice age.