PRKCB and diabetic cardiomyopathy: Transgenic mice with cardiac-specific overexpression of PKCβ displayed heart enlargement, dysfunction, fibrosis, and early mortality.[110–112] Although not essential, as PKCβ-null mice showed similar hypertrophic responses to stress as wild-type mice,[113] inhibition of PKCβ, as shown in a rat model of diabetic cardiomyopathy, reduced myocyte hypertrophy and fibrosis.[114]