It has demonstrated protective effects on HDL and apoA-I against proteolytic degradation caused by glycation and oxidation, specifically, CIGB-258 dose-dependent protection for HDL and apoA-I from CML-induced glycation by stabilizing their protein structure and enhancing their antioxidant capacity. This evidence concerns the gene APOA1 and chronic myelogenous leukemia, BCR-ABL1 positive.