While according to our model a balanced abundance of TIP30 and its target eEF1A1 enables compensated cardiac growth during pathological overload, a reduced myocardial TIP30/eEF1A1 ratio like in the late stage of human heart failure promotes exaggerated cardiomyocyte growth and ventricular dysfunction, which could arise from insufficient concomitant myocardial capillary growth. This evidence concerns the gene EEF1A1 and heart failure.