In response to AngII infusion, Klf15 deficient mice develop a severe aortapathy characterized by elastolysis, increased apoptosis and reduced medial thickness, and cardiomyopathy characterized by left ventricular dysfunction compared to AngII-induced wildtype mice indicating Klf15 deficient mice are more susceptible to develop stress-induced cardiovascular pathologies. This evidence concerns the gene AGT and cardiomyopathy.