fig3

Gene therapy for inborn errors of immunity: past progress, current status and future directions

Figure 3. Mechanisms of repair of a dsDNA break. Following generation of a DSB by a CRISPR/Cas nuclease, the lesion is typically either repaired by either non-homologous end joining, which is highly error prone and often leads to gene disruption, or by homology-directed repair which can lead to precise edits at the cut site. Created in BioRender. Orf K (2025) https://BioRender.com/kfj1a7h. CRISPR: Clustered regularly interspaced short palindromic repeats; dsDNA: double-stranded DNA; DSBs: double-strand DNA breaks.

Rare Disease and Orphan Drugs Journal
ISSN 2771-2893 (Online)
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