More importantly, the human cardiac cell would allow pilot drug-screening studies on targeting oxidative stress signaling in cardiac laminopathy, clearance of misfolded lamin proteins, delay in the rate of producing toxic farnesylated lamin, arising from mutation at cleavage sites of prelamin A/C protein, the blockade of stress-related MEK1–Erk1/2, JNK, and p38-mediated MAPK pathways, or even the cardiac protective microRNA (miR) that reduces prelamin A accumulation. This evidence concerns the gene LMNA and laminopathy.