In non-diabetic dyslipidemic mice (Apoe-knockout mouse), treatment with AGE-albumin increased lipid deposition in the aortic arch, enhanced the expression of Ager, Tnf (tumor necrosis factor) and Nox4 (NADPH oxidase 4) genes, and increased the marker of lipid peroxidation (4-hydroxynonenal) and CML, in comparison with animals receiving control-albumin. The gene discussed is AGER; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.