We also found deletions in apeh, an enzyme that destroys oxidatively damaged proteins [53]; trim39, a tripartite motif involved in erythropoiesis [54] and slc25a42, a mitochondrial transporter of coenzyme A [55] associated with mitochondrial myopathy and lactic acidosis in humans [56]. The gene discussed is APEH; the disease is Mitochondrial myopathy.