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In the early, online edition of Proceedings of the National Academy of Sciences, investigators from the University of Massachusetts and Tufts University demonstrate the feasibility of establishing a mouse model of genetically-induced emphysema using CRISPR/Cas9-based editing to lop out half a dozen paralogs of Serpina1 — a gene implicated in alpha-1 antitrypsin deficiency (AAT)-related forms of emphysema in humans.

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