TrkB.T1 is also capable of enhancing downstream targets of PDGF signaling in vitro, including Akt, STAT3, and pS6 (Fig. 5), and future studies should explore if this is a PDGF-specific effect or a more general effect of TrkB.T1 exhibiting crosstalk with other receptor tyrosine kinases to explore whether this phenomenon may be applicable to other tumor types beyond gliomas. The gene discussed is AKT1; the disease is neoplasm.