Among them, suppression of mTor, Mapk, Pdgf signaling pathways, inhibition of BET bromodomain, or disruption of lamina-cytoskeleton links have been proposed to suppress or ameliorate LMNA DCM by using various models including global/cardiac specific knockouts, LMNA mutants as well as patient specific iPS derived cardiomyocytes [6, 7, 11–13]. This evidence concerns the gene MTOR and familial dilated cardiomyopathy.