Bringing the activated coagulation factor IXa (FIXa) in close vicinity to factor X (FX) enables the FIXa-mediated proteolytic activation of FX to FXa; this is usually the function of FVIII, which is absent in hemophilia A. Emicizumab was designed by engineering a common light chain (CDR1 and CDR3 bind to FIXa, and CDR2 binds to FX) and by engineering differentially mutated heavy chains to favor heterodimers via electric repulsion and attraction, called ART-Ig (asymmetric reengineering technology-immunoglobulin) [158,159]. This evidence concerns the gene F10 and hemophilia A.