In renal tubular epithelial cells, the primary target in AKI—hypoxia-reoxygenation injury induces necroptosis, characterized by increased RIP1/RIP3 interaction and necrosome assembly, which can be attenuated by the RIPK1 inhibitor Necrostatin-1 (Zhu et al., 2018). This evidence concerns the gene RIPK3 and acute kidney injury.