ACAD10 (acyl-CoA dehydrogenase family member 10) is a mitochondrial enzyme with dual catalytic domains that enables the catabolism of 4-hydroxy fatty acids, a previously unexplored class of lipid metabolites 1. Unlike conventional acyl-CoA dehydrogenases, ACAD10 uniquely combines kinase and dehydrogenase activities: it phosphorylates 4-hydroxyacyl-CoAs at the 4-position via its N-terminal kinase domain, then eliminates the phosphate through its C-terminal ACAD domain to generate conventional 2-enoyl-CoAs compatible with β-oxidation 2. ACAD10 preferentially metabolizes shorter-chain 4-hydroxy fatty acids (≤6 carbons) relative to its peroxisomal homolog ACAD11 1. Functionally, ACAD10 localizes to mitochondria and also peroxisomes across multiple tissues 3, with broad expression in liver, kidney, pancreas, and brain 4. Clinically, ACAD10 deficiency impairs glucose tolerance and causes peripheral insulin resistance, implicating it as a genetic determinant of type 2 diabetes mellitus 5. Knockout mice exhibit abnormal weight gain, elevated fasting acylcarnitines indicative of impaired fatty acid oxidation, fasting-induced rhabdomyolysis, and hepatic inflammation 3. Additionally, ACAD10 shows elevated expression following metformin treatment 6, suggesting therapeutic potential. Genome-wide analyses identify ACAD10 as a pleiotropic locus shared between telomere length and cardiovascular disease susceptibility 7.