The overexpression of SET contributes to the tumor cell proliferation, metastasis, and drug resistance [29]; on the other hand, the knockdown of SET or the administration of the SET antagonist fingolimod (FTY720), thereby restoring PP2A antitumor activity, reduces the clonogenic and tumorigenic potential in vitro and in vivo [19,30,31]. Here, SET is linked to neoplasm.