In addition, FGFR inhibitors - NVP-BGJ398 and PD173074, with selectivity against FGFRs, and dovitinib (TKI258), targeting also Vascular Endothelial Growth Factor Receptors (VEGFRs), Platelet Derived Growth Factor Receptors (PDGFRs), FLT3 and c-Kit [16] - were shown to exert anti-tumor activity by hampering glucose metabolism through AKT/mTOR inhibition. The gene discussed is AKT1; the disease is neoplasm.