In an adult mouse study of middle cerebral artery occlusion (MCAO), C3 deficiency and site-targeted inhibition with either CR2-Crry (inhibiting all pathways) or CR2-fH (inhibiting AP) significantly reduced infarct size, reduced apoptotic cell death, and improved neurological deficit score in the acute phase after stroke, but only CR2-fH provided sustained protection with no further development of injury in the subacute phase (52). The gene discussed is C3; the disease is stroke disorder.