Consistent with these findings, present research indicates that mindin overexpression promotes p65 translocation from the cytoplasm into the nucleus, leading to NF‐κB pathway activation in vitro, while mindin disruption deactivates the NF‐κB pathway in mice after renal IRI; this suggests that mindin might exacerbate renal damage, at least partially, through regulating the NF‐κB signalling pathway in the progress of renal fibrosis. The gene discussed is SPON2; the disease is renal fibrosis.