When everolimus (an orally administered inhibitor of mTOR) was used to treat a mouse model [Pten (tm1Hwu/tmiHwu); Ctnnb1 (tm1Mmt/+); Amhr2 (tm3(cre)Bhr/+] in which mTOR, RPS6KB1, eIF4B, and PPARG are upregulated in tumor cells similar to human GCTs, investigators were unable to fully reverse the molecular consequences of mTOR activation despite the fact that the use of everolimus slowed tumor growth (Rico et al., 2012). This evidence concerns the gene RPS6KB1 and neoplasm.