LXR agonists bind to nuclear receptors, increase the expression of cholesterol efflux transporters ABCA1 and ABCG1, and trigger the degradation of LDLR through upregulation of IDOL E3 ligase.[13, 14, 16, 17, 18] These mechanisms all work in concert to lower intracellular cholesterol levels, deprive the tumor cells of cholesterol and trigger tumor cell death in GBM. This evidence concerns the gene ABCA1 and neoplasm.