In this issue of Circulation Research, Zhang et al1 provide direct and clear evidence that phosphorylation of S2808 in the cardiac ryanodine receptors (RyR2) has no impact on either normal cardiac function, sympathetic stimulation of the heart, or progression of heart failure (HF) after myocardial infarction (MI). They used mice in which the S2808 site was rendered nonphosphorylatable in S2808A knock-in mice, and the results directly contradict results published by the group of AR Marks. 2–4 This has been a highly controversial area. This new study compels me to assess this pathway in a balanced way, but recognizing that my opinions are influenced by work that my group has done in this area. My goal here is not to microdissect each controversial piece of data in dozens of relevant papers (see recent reviews and tables5, 6), but rather to provide my informed opinion about key aspects of this issue in a balanced manner. Let us first consider the model that importantly raised the issue of SR Ca leak as a potential pathophysiological cardiac effect in HF.