ETFB (electron transfer flavoprotein subunit beta) is a critical mitochondrial matrix protein that functions as the β-subunit of the heterodimeric electron transfer flavoprotein complex. ETFB accepts electrons from multiple mitochondrial dehydrogenases, including acyl-CoA dehydrogenases and sarcosine dehydrogenase, transferring them to the main respiratory chain via ETF-ubiquinone oxidoreductase 1. This electron shuttle activity is essential for normal mitochondrial fatty acid oxidation and amino acid catabolism. ETFB contains a structurally important bound AMP molecule 1. Deficiency of ETFB causes glutaric acidemia type II (glutaric aciduria 2B), an inherited metabolic disorder characterized by severe hypoketotic hypoglycemia, acidosis, and potential neonatal fatality 1. ETFB emerges as a relevant biomarker in diverse pathological contexts: elevated ETFB levels correlate with worse renal dysfunction in congenital hydronephrosis 2, serve as a diagnostic marker for leptospiral infection 3, and predict poor overall survival in acute myeloid leukemia patients 4. Proteomically, decreased ETFB in cerebrospinal fluid and cortex associates with mitochondrial dysfunction in Alzheimer's disease, highlighting broader neurological relevance 5. Additionally, ETFB-related metabolic disorders respond to riboflavin supplementation, reflecting the protein's flavin-dependent function 6.