Zhongwei Liu (Liu et al., 2014) et al. showed that in DCM rats treated with ERS inhibitor 4-phenylacetic acid, the expression of ERS chaperone GRP78 was reduced, which inhibited ERS and decreased the number of premature beats, again proving that ERS was associated with arrhythmias in DCM, and further studies showed that PERK was a mediator; Using RNAi technology, the team confirmed that PERK in ERS could increase the activity of calmodulin neuralphosphatase, which induced increased Ca2+ in cardiomyocytes and led to arrhythmias. This evidence concerns the gene EIF2AK3 and cardiac arrhythmia.