Result: In PARK9 model cell, expression of iron-related genes such as Transferrin Receptor (TfR) was increased, suggesting the disruption of iron homeostasis. To examine iron homeostasis, we focus on the capacity of heme synthesize. Heme is known to play a role in regulating intracellular iron concentration. The ability to heme synthesizes was decreased in PARK9 model cells. Since heme is synthesized in mitochondria, it is assumed that mitochondrial disorders are involved in the reduction of heme synthesis. Therefore, it is possible that mitochondrial dysfunction may be a factor in the abnormal intracellular iron homeostasis in PARK9 model cells. In addition, we found dysfunction of mitophagy, suggesting that accumulation of damaged mitochondria.