Ataxia–telangiectasia (A–T) is an autosomal recessive disorder characterized by cerebellar ataxia and oculocutaneous telangiectasias. The gene mutated in this disease, Atm (A–T mutated), encodes a serine/threonine protein kinase that has been traditionally considered to be a nuclear protein controlling cellcycle progression. However, many of the growth abnormalities observed in patients with A–T, including neuronal degeneration and insulin resistance, remain difficult to explain with nuclear localization of ATM.