To investigate whether TNF-α inhibition prevents the development of kidney fibrosis, and to elucidate the underlying molecular mechanisms, we evaluated the effects of etanercept (ETN), which is a fusion protein competitively acting as a "TNF-α decoy receptor" to inhibit the binding of TNF-α to its cell surface receptor34, on kidney functional decline, inflammation, and fibrosis in a murine model of AAN. The gene discussed is TNF; the disease is Balkan nephropathy.