Imai rats, a model of spontaneous focal glomerulosclerosis, exhibit heavy proteinuria, hypoalbuminemia, hypertension, azotemia, glomerulosclerosis, tubulointerstitial inflammation, increased angiotensin II expressing cell population, up-regulations of AT1 receptor, AT2 receptor, NAD(P)H oxidase, and inflammatory mediators, activation of NF-κB, and reduction in NRF2 activity and its downstream gene expressions in the renal cortex. The gene discussed is NFKB1; the disease is glomerulosclerosis.