Furthermore, we expect to confirm in future studies that blockade of cathepsin B (which would decrease LG3 levels, [37, 38]) would mitigate or prevent IL-1α neuroprotection in vitro, and that post-stroke administration of IL-1α also increases brain LG3 levels in wild-type mice in vivo which would further support the importance of LG3 in the therapeutic mechanism of action of IL-1α. The gene discussed is IL1A; the disease is Stroke.