For example, Goeb and colleagues demonstrated that genetic depletion of plasma kallikrein as well as targeted inhibition of plasma kallikrein via an antibody reduced infarct volume and improved neurological parameters following murine tMCAO [14], whilst antibody-mediated inhibition of FXI [50] as well as kininogen deficiency [49] likewise improved outcome following ischemic stroke in mice. This evidence concerns the gene KLK4 and ischemic stroke.