NFKB1 and nephritis: Thus, tPA/LRP-1 signaling may also indirectly activate the NF-κB pathway through p90RSK-mediated IκB phosphorylation and further amplify NF-κB-dependent proinflammatory signaling, such as the macrophage M2-to-M1 phenotypic switch, resulting in a vicious loop of amplification and excessive kidney inflammation.