Because DAPK1 inhibitor also blocks the hypoxia-dependent Pellino1 Ser39 phosphorylation, caspase-8 recruitment of TRIF-RIP1 signalosome and tubular apoptosis during LPS stimuli, it is possible that pharmacological deactivation or genetic ablation of DAPK1 protects mice from septic AKI via controlling these events. This evidence concerns the gene RIPK1 and acute kidney injury.