Thus, the beneficialactions of insulin in diabetic nephropathy appear to be mediated, in part, bysuppressing renal Nrf2 and Agt gene transcriptionand preventing Nrf2 stimulation of Agt expression via hnRNP F/K.These findings identify hnRNP F/K and Nrf2 as potential therapeutic targets indiabetes. The gene discussed is INS; the disease is diabetic kidney disease.