These mutations reduce both the molecular weight and the immunogenicity of SAK-HV, which was developed as a novel anti-atherosclerosis drug candidate, and has been shown to have multiple functions, including fibrinolysis triggered by SAK-mutant, anti-coagulation exerted by hirudin-12, and the inhibition of platelet aggregation induced by RGD [24]. This evidence concerns the gene PLK4 and atherosclerosis.