In the treatment of DCM caused by defects in fission genes, therapy may not only target fission, with drugs like LCZ696 (a novel angiotensin receptor neprilysin inhibitor) or Drp1-specific inhibitors like Midivi-1 (91), but also employ drugs that modulate fusion proteins (e.g., MFN2 agonists). This evidence concerns the gene MFN2 and familial dilated cardiomyopathy.