Collateral vessel recruitment after AIS is rapid, occurring on the order of seconds in rodent studies.16 In addition to collateral recruitment, administering KLK1 reportedly improved long-term perfusion by enhancing the spontaneous processes of collateral remodeling and new collateral formation, as evidenced in experimental AIS models.17–19 The collateralization process encompasses 3 distinct but mutually synergic mechanisms: angiogenesis, vasculogenesis, and arteriogenesis. The gene discussed is KLK1; the disease is androgen insensitivity syndrome.