PLN and heart failure: In this context, gene therapeutic approaches for inhibiting PLB expression by employment of dominant-negative PLB mutants [7], intracellular inhibitory antibodies targeting PLB [8] or engineered zinc-finger protein transcription factors (ZFP TFs) to the endogenous PLB gene [9] have been shown to improve the SERCA2a-catalyzed Ca2+ transport activity in cardiomyocytes and the contractile function of the heart in animals models of heart failure.