In exploring ERRα’s role in DKD, we utilized two established diabetes models: the db/db mouse model at 16 weeks of age with a BKS genetic background and the STZ‐induced model, created through 16‐week post‐intraperitoneal streptozotocin injection.[16] Both models demonstrated a marked reduction of ERRα expression within kidney tissues, compared to their respective controls (db/m mice or those receiving citrate buffer injections), as evident in immunofluorescence and immunohistochemistry analyses (Figure2A–D; Figure S2A–D, Supporting Information). The gene discussed is ESRRA; the disease is diabetic kidney disease.