In conclusion, by integrated analysis of different high-throughput data and validation, we identified several crucial genes in AKI, such as Havcr1, Krt20, Sox9, Egr1, Timp1, Serpine1, Edn1, and Apln; they might have cofunctions, and their dysregulations might alter activities of pathways such as positive regulation of cell proliferation, complement and coagulation cascades, and TNF signaling, which might finally promote AKI progression. This evidence concerns the gene APLN and acute kidney injury.