Cas9 in Human Embryos: On Target but No Repair

Eva R. Hoffmann*, Ignasi Roig

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

4 Citations (Scopus)

Abstract

In this issue of Cell, Zuccaro and colleagues show that on-target Cas9-mediated double-strand breaks cause chromosome loss or mis-repair of the disease allele in > 90% of human embryos. End joining repair pathways dominate, causing small insertions or deletions, which raises serious questions about using double-strand breaks for “gene surgery”.

Original languageEnglish
Pages (from-to)1464-1466
Number of pages3
JournalCell
Volume183
Issue number6
DOIs
Publication statusPublished - 10 Dec 2020

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