Although reduced PLB phosphorylation is regarded as an important mechanism of lower SERCA2a activity in HF, conflicting results exist from both animal models and the limited work done in human HF; human data from explanted dilated cardiomyopathy hearts with terminal HF found both Ser‐16 and Thr‐17 phosphorylations of PLB to be reduced,15, 16 but a later report found only Ser‐16, but not Thr‐17, phosphorylation to be reduced.17 The gene discussed is PLN; the disease is hydrops fetalis.