As shown in Figure 6, our present work, based on our previous finding that annexin A2 acts as co-receptor of CD 11b to activate ILK-mediated signaling [12], demonstrates that tPA modulates macrophage M2 to M1 phenotypic change through annexin A2-mediated ILK activation, which in turn phosphorylates IκB and activates NF-κB, contributing to the accumulation of M1 macrophages and resultant increased renal inflammation. The gene discussed is NFKB1; the disease is inflammatory response.