Moreover, knockout of calpain in endothelial cells may confer protective effects in LPS-induced AKI by inhibiting p38 phosphorylation and diminishing the expression of inducible nitric oxide synthase (iNOS), and further decreasing endothelial cell apoptosis caused by excessive NO/ROS production (Liu et al., 2020) (Figure 2). The gene discussed is NOS2; the disease is acute kidney injury.