ATP7A is an ATP-driven copper transporter that maintains intracellular copper homeostasis through active Cu(+) ion pumping across cellular membranes 123. The protein operates as a P-type ATPase, acquiring Cu(+) from cytoplasmic donor proteins and transferring it across the membrane via ATP hydrolysis-coupled phosphorylation, which induces conformational shifts from inward-facing to outward-facing states 456. Under normal copper levels, ATP7A localizes to the trans-Golgi network, delivering Cu(+) to cuproenzymes including tyrosinase and cytochrome oxidase 23. Upon copper elevation, it relocates to the plasma membrane to export excess copper, protecting cells from oxidative stress 17. ATP7A mutations cause Menkes disease, a lethal X-linked disorder characterized by neurodegeneration, connective tissue defects, and early mortality without treatment 8. Clinical phenotypes include classical Menkes disease with early seizures, atypical variants with ataxia, and occipital horn syndrome with milder presentations 9. Beyond genetic disease, cancer cells exploit ATP7A-mediated copper handling; targeting ATP7A degradation enhances ferroptosis and cuproptosis in colorectal, breast, and lung cancers, offering therapeutic opportunities 101112.