The definitive guide to gene editing.
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Gene · Cardiovascular

PCSK9

Proprotein convertase subtilisin/kexin type 9 — A liver gene that controls how much LDL cholesterol stays in the blood — and the target of the first attempt to treat a common chronic disease with a one-time edit.

1p32.3 cholesterolin vivobase editing
Chromosome 1 PCSK9 1p32.3 p q

Schematic only — arm proportions are approximate and band detail is not drawn to scale. Cytogenetic location as published by NCBI Gene.

What this gene does

Liver cells pull LDL cholesterol out of the blood using receptors on their surface. PCSK9 destroys those receptors, so more cholesterol stays in circulation. People born with a broken PCSK9 gene have low cholesterol and appear entirely healthy — which is exactly why it is such an attractive target: nature has already run the experiment.

PCSK9, at 1p32.3, encodes a protease that binds the LDL receptor and directs it to lysosomal degradation, reducing hepatic LDL clearance. Loss-of-function variants are associated with lifelong low LDL cholesterol and reduced cardiovascular events without evident harm; gain-of-function variants cause familial hypercholesterolemia. It is validated as a drug target by approved monoclonal antibodies and siRNA medicines, and is the target of in vivo base-editing programmes intended to make the effect permanent.

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