We have also shown that HuR expression and cytoplasmic translocation, an indicator of RNA binding activity, is increased in failing human hearts and that both cardiomyocyte-specific ablation or pharmacological inhibition of HuR reduces the progression of cardiac hypertrophy and fibrosis in a pressure overload (transverse aortic constriction; TAC) model of heart failure (Green et al., 2019). The gene discussed is ELAVL1; the disease is heart failure.