While with AGT and renin the renal abundances of two major components of the local RAS increased in AAI-induced nephropathy, matching similar experimental [23, 27, 51, 62] and clinical observations [4, 23, 64] in other types of chronic nephropathy, renal ACE abundance, and activity in wildtype mice decreased to about half of their baseline values. The gene discussed is AGT; the disease is kidney disorder.