Our present study expands on the already established cardioprotective role of RGS4, which is upregulated, most likely as a compensatory mechanism, in the hearts of experimental animals of cardiac hypertrophy secondary to aortic or pulmonary artery banding in vivo [19] and in human failing hearts explanted from dilated or ischemic cardiomyopathy patients, or from end-stage or acute human heart failure patients [10,20,21]. This evidence concerns the gene RGS4 and ischemic cardiomyopathy.