In addition, Glo1 knockout mice were susceptible to acetaminophen-induced hepatotoxicity [47]; Glo1 knockdown mice had a diabetic-nephropathy-like phenotype [48], while the manipulation of GLO1 activity did not alter the atherosclerotic burden in atherosclerosis-prone Apoe-/- mice [49]. This evidence concerns the gene APOE and atherosclerosis.