Self-phosphorylated CaMKII can be dephosphorylated by protein phosphatases (including PP1 or PP2A) to restore the self-inhibited state, which are potential targets in cardiac disease like HF, arrhythmia, and MI (Strack et al., 1997; Fischer et al., 2018; El Refaey et al., 2019). This evidence concerns the gene CAMK2G and hydrops fetalis.