Importantly, our data demonstrating that Mac-1 deficiency dramatically reduces spontaneous ICH associated with late thrombolysis are consistent with our earlier study showing that PDGFRα antagonists can reduce thrombolysis-associated ICH [61, 69, 70] and support the idea that targeting PDGFRα signaling in stroke has the potential to significantly improve the safety of thrombolytic therapy. The gene discussed is PDGFRA; the disease is stroke disorder.