GLYCTK encodes glycerate kinase, a mitochondrial enzyme 1 that catalyzes protein phosphorylation in serine and fructose metabolism 2. The enzyme localizes exclusively to mitochondria 1, where it phosphorylates D-glycerate as part of normal metabolic pathways 3. GLYCTK deficiency causes D-glyceric aciduria (DGA), a rare autosomal-recessive inborn error of metabolism characterized by elevated urinary D-glyceric acid 2. Clinical presentations are highly variable, ranging from severe neurological symptoms including muscular hypotonia, joint hypermobility, and tremor 2 to asymptomatic cases, suggesting disease heterogeneity 1. Pathogenic mutations in GLYCTK include frameshift and missense variants that result in loss of enzyme activity and immunoreactivity 3. Beyond classical metabolic disease, GLYCTK variants show emerging associations with complex traits. Reduced GLYCTK expression in hippocampal tissue is linked to oscillatory brain activity variations affecting alpha power and psychiatric risk 4. GLYCTK expression is also protective against diabetic kidney disease, with downregulation observed in podocytes and tubular cells in affected kidneys 5. Additionally, GLYCTK expression variations are associated with anxiety disorder risk through cis-regulated expression mechanisms 6, indicating pleiotropic effects beyond its primary metabolic role.