Using CRISPR-based genome editing technology and a proprietary nuclease, a group of researchers was able to successfully delete the 2.5 kb 3′UTR region of the LDLR gene in an FH patient-derived lymphoblastoid cell line and in mice that resulted in increased LDLR mRNA, protein and activity [211] (Figure 5), similar to that observed in human carriers lacking this same 2.5 kb 3′UTR region of the LDLR gene [194]. Here, LDLR is linked to familial hyperaldosteronism.