Since podocytes express both the C3a receptor and TLR4, we speculate that complement C3a may activate the TLR4 protein of glomerular podocytes through the TLR4/NFκB-P65 signaling pathway, inducing NFκB-P65 nuclear translocation, participating in the inflammation and transdifferentiation of glomerular podocytes and resulting in the progression of post-AKI renal fibrosis. The gene discussed is NFKB1; the disease is acute kidney injury.