Another study has reported that reduction in TTN and lamin A/C triggered by NMD can reduce cardiac metabolism of medium and long chain fatty acids, thereby increasing cardiac glycolysis dependency which could consequently increase activation of mammalian target of rapamycin target (mTORC1) signaling pathway [95], hence promoting ineffective protein synthesis and autophagy leading to myocardial damage, myocardial contraction disorder, and formation of DCM [96]. The gene discussed is LMNA; the disease is familial dilated cardiomyopathy.