CAMK2G and heart failure: Mustroph et al. (6) showed that empagliflozin reduced calcium/calmodulin-dependent protein kinase II (CaMK II) activity and CaMK II-dependent ryanodine receptor phosphorylation in the cardiomyocytes of mice with heart failure model; empagliflozin also reduced the human cardiomyocyte Ca2+ spark (CaS) frequency but increased the sarcoplasmic reticulum Ca2+ ([Ca2+]SR) levels and Ca2+ transient (CaT) amplitude, whereas CaMK II overexpression and Ca2+-dependent activation were the main causes of arrhythmogenesis.