Because we observed that there was a deregulation in the NAD+/NADH ratio and an increase in the acetylated lysines in heart proteins during CRS-4 and because recent research has proposed that NAC can modulate mitochondrial redox homeostasis through the adenosine monophosphate (AMP)-activated protein kinase alpha (AMPKα)- peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)-SIRT3-SOD2 pathway in renal and acute cardiorenal disease [21,22,23], we investigated whether this signaling pathway was also modified in the heart’s mitochondria. The gene discussed is SOD2; the disease is craniosynostosis 4.