Further genetic modifications included transgenic overexpression of human proteins to decrease cellular injury (CD47 and Hemoxygenase 1) (Petersen et al., 2010; Ahrens et al., 2015; Cooper et al., 2018), complement activation (hCD55 and hCD46) (Fischer et al., 2016) and coagulopathies (human Endothelial Cell Protein C Receptor and human Thrombomodulin) (Oropeza et al., 2009; Petersen et al., 2009). This evidence concerns the gene THBD and blood coagulation disease.