SLC25A39 is a mitochondrial inner membrane transporter that serves as the primary mechanism for glutathione (GSH) import into mitochondria 1. This transporter is essential for maintaining mitochondrial GSH levels, which are critical for the activity and stability of iron-sulfur cluster-containing proteins and for erythropoiesis 1. SLC25A39 operates under sophisticated autoregulatory control: under normal conditions, it is rapidly degraded by the mitochondrial protease AFG3L2, but GSH depletion causes AFG3L2 to dissociate from SLC25A39, leading to increased transporter stability and compensatory GSH uptake 2. The transporter contains a putative iron-sulfur cluster in its matrix-facing loop that is essential for this regulation, directly coupling mitochondrial iron homeostasis to GSH import 2. Loss of SLC25A39 impairs cellular functions including proliferation and red blood cell development 1. Clinically, SLC25A39 has been implicated in cancer progression, where it enables cuproptosis resistance in pancreatic cancer 3 and is required for breast cancer metastatic colonization through integrated stress response signaling 4. Additionally, rare variants in SLC25A39 have been identified as potential risk factors for late-onset Parkinson's disease 5.