Overexpression of HSPB8 promotes cardiomyocyte survival after ischemia in mice (Depre et al. 2006) and attenuates the myocardial damage and contractile dysfunction in pig (Chen et al. 2011), whereas depletion of HSPB8 in mice with pressure overload contributes to the cardiac dysfunction and accelerates transition to heart failure (Qiu et al. 2011). This evidence concerns the gene HSPB8 and heart failure.