For example, there is a significant biological and ethical difference between a “correction” of a rare, disease-associated mutation to a widespread non-pathogenic allele as is being investigated for HBB and MYBPC3 in the case of β-thalassemia and hypertrophic cardiomyopathy respectively, and attempted edits to CCR5 with its complex, multiple phenotypic effects and potentially pathogenic off-target effects (97, 98). This evidence concerns the gene CCR5 and hypertrophic cardiomyopathy.