To establish causality, a podocyte-specific Cldn5 knockout was generated in STZ-induced DN mice, revealing that loss of Cldn5 heightened susceptibility to diabetic kidney injury, as evidenced by early-onset albuminuria (at 4 weeks) and glomerulosclerosis (at 12 weeks) [159]. The gene discussed is CLDN5; the disease is liver dysplastic nodule.