Hyperactivity of RyR in cardiac disease is often attributed to posttranslational modifications, including phosphorylation of PKA- and CaMKII-specific sites, and oxidation of many reactive cysteines within the protein (Györke and Carnes, 2008; Niggli et al., 2013; Zima et al., 2014). The gene discussed is CAMK2G; the disease is heart disorder.