TNF-α and other pro-inflammatory cytokines can activate calcium/calmodulin-dependent protein kinase alpha (CaMKα) and the following NF-κB pro-inflammation pathway.77,92 High concentrations of TNF-α decrease calcium transients and attenuate cardiomyocyte contraction.93 IL-1 can activate ryanodine receptor (RyR) and release calcium from the sarcoplasmic reticulum, which causes intracellular calcium overload and deteriorates the excitation-contraction coupling process.94 Together, these changes will contribute to the development of arrhythmias. This evidence concerns the gene TNF and cardiac arrhythmia.