SFXN2 (sideroflexin 2) is a mitochondrial transmembrane protein that functions as an amino acid transporter mediating serine import into mitochondria 1. Its primary role involves regulating mitochondrial iron homeostasis by controlling heme biosynthesis 2. SFXN2 knockout cells exhibit elevated mitochondrial iron accumulation with decreased heme content and heme-dependent enzyme activities, ultimately impairing mitochondrial respiration 2. The protein also suppresses mitochondrial autophagy and mitophagy while promoting iron-mediated energy production to support cell proliferation 3. In disease contexts, SFXN2 dysregulation has emerging clinical significance. In multiple myeloma, elevated SFXN2 expression correlates with poor outcomes and promotes proliferation through mitochondrial bioenergetics and iron metabolism regulation 3, while kaempferol-induced SFXN2 downregulation triggers apoptosis through iron dysregulation and mitophagy 4. In breast cancer, high SFXN2 expression associates with favorable prognosis, contrasting with other family members 5. Cross-ancestry genome-wide association studies identified SFXN2 as a schizophrenia risk gene missed in European-only datasets 6. SFXN2 also appears relevant to chr10 kidney disease progression as part of predictive gene panels 7. These findings establish SFXN2 as a critical regulator of mitochondrial metabolism with diverse roles in cancer and neuropsychiatric disease.