In light of the evidence connecting PGAM5 and PHB2 with mitochondrial dysfunction and metabolic anomalies commonly observed in DCM, as well as the bioinformatics analysis predicting a potential interaction between these proteins, we tested the hypothesis that PGAM5-mediated dephosphorylation of PHB2 disrupts MQS to aggravate myocardial dysfunction in DCM. Here, PGAM5 is linked to familial dilated cardiomyopathy.