GFOD1 (Gfo/Idh/MocA-like oxidoreductase domain containing 1) is a catalytically inactive oxidoreductase that does not bind NAD or NADP cofactors but appears to play important regulatory roles in neurological function and disease. The protein is expressed in the central nervous system during embryonic, larval, and adult stages, with specific expression in GABAergic neurons 1. GFOD1's primary mechanism involves regulation of oxidative stress through the NF-κB signaling pathway. In ADHD models, GFOD1 overexpression activates the NF-κB p65/NOX2 signaling pathway, leading to increased reactive oxygen species (ROS) and malondialdehyde levels while reducing superoxide dismutase activity 2. Disease relevance includes associations with psychiatric conditions, particularly ADHD, where polymorphisms in GFOD1 correlate with inattentive symptomatology 1. GFOD1 expression is elevated in ADHD rat models, specifically in prefrontal and cerebellar cortices 2. Clinical significance extends beyond neuropsychiatric disorders, as GFOD1 is upregulated in clear cell renal cell carcinoma and correlates with disease progression and poor prognosis 3. Additionally, GFOD1 has been identified as a potential biomarker for acute myocardial infarction 4 and is involved in NTRK fusion events in certain cancers 5.