Interestingly, LCC-09 not only demonstrated significant suppression of RANKL- and, by inference, NF-κB-mediated GSC phenotypes, but also elicited a very strong inhibitory effect on the expression levels of dopamine receptors 2 (DRD2), and 4 (DRD4) proteins, CDK6, β-catenin, and Akt/mTOR, all of which are implicated in GBM mitogenic signaling and expansion of the GSC [17,18]. The gene discussed is MTOR; the disease is glioblastoma.