In contrast, glioma tumor initiating cells plated at high density maintain cholesterol at levels compatible with cell proliferation and viability by (1) keeping de novo synthesis on through the mevalonate pathway and by (2) activating LXRβ to upregulate cholesterol efflux through ABCA1 and pathways involved in lipid metabolism and immune regulation (Fig. 8B). This evidence concerns the gene ABCA1 and glioma.