It seems likely that the effects of TKI drugs may extend to other phosphorylated receptors found to be altered in chordomas, such as PDGFR-a [40], and to kinases that participate in additional pathways, such as Akt and mTOR, whose targets, TSC2 and the translation initiation factor binding protein EIF4EBP1, are found in a phosphorylated state in chordoma cells [41]. The gene discussed is PDGFRA; the disease is chordoma.