Although many studies have shown that activating LXR is an effective target for killing GBM cells, Patel et al. have found that LXRβ maintains the cholesterol homeostasis of GBM cells during high-density growth in vitro by upregulating ABCA1 and inhibiting the mevalonate pathway and that LXRβ maintains the cell viability during high-density growth in an ABCA1-independent manner. This evidence concerns the gene NR1H2 and glioblastoma.