PLB inhibition is relieved by phosphorylation either by CaMKII or protein kinase A. Numerous subsequent studies, including our own, have shown P-PLB(Thr17) to be briefly elevated in early ischemia, peaking in the initial 1–3 min of reperfusion (Vittone et al., 2002; Said et al., 2003; Valverde et al., 2006; Vila-Petroff et al., 2007; Salas et al., 2010) at a time when hypercontracture and ventricular arrhythmias are prevalent, before rapidly returning to basal activation level. The gene discussed is PLN; the disease is Ventricular arrhythmia.