Furthermore, fibroblasts from sPD patients treated with AntiOxCIN4 showed increased TFAM and TFB2m mRNA levels, possibly as a compensatory mechanism in response to decreased mtDNA copy number and/or to a more efficient regulation of mtDNA structural stability, since TFAM and TFB2m determine the abundance of the mitochondrial genome by regulating packaging, stability, and replication [72,73]. The gene discussed is TFAM; the disease is Platelet storage pool disease.