However, the situation becomes detrimental if RyR2 is hypersensitive to activation in disorders such as catecholaminergic polymorphic ventricular tachycardia or if the redox potential is further increased and the degree of thiol modification is increased with NOX2 stimulation and excess ROS production as a result of chronic β adrenergic stimulation, as in heart failure (Sánchez et al., 2005; Zhang et al., 2013). This evidence concerns the gene RYR2 and heart failure.