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One-shot, one cure with genome editing for dyslipidemia.

One of the most inspiring examples of rapid bench-to-bedside translation has been the development of proprotein convertase subtilisin/kexin 9 (PCSK9) inhibitory antibodies for the reduction of serum low-density lipoprotein and prevention of coronary artery disease. Astute genetic analysis of gain-of-function mutations in patients with elevated low-density lipoprotein (LDL) levels1 built the case for the role of PCSK9 in LDL receptor binding and lysosomal destruction.2 Now the prospect of lipid-lowering therapy delivered monthly via injection is on the horizon with successful clinical trials for the 2 leading monoclonal antibodies.3 The logical next expectation would be for a permanent disruption of the PCSK9 gene, rendering continued therapy unnecessary because the naturally occurring and protective loss-of-function mutation could be given as a 1-time treatment. Ding et al4 present evidence that the technology for this now exists with genome editing and the clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated (Cas) …