Many studies have shown the subtleties involved in utilizing CRISPR-Cas as a mechanism for modifying genes associated with hemophilia A or B. In these investigations, the clotting factor gene deficiency was either fixed in situ, or the strong albumin promoter was hijacked to drive FVIII or FIX by using the albumin locus as a haven [109]. This evidence concerns the gene ALB and hemophilia A.