Inhibition of EGFR (NSCLC) and RET (medullary thyroid cancer) tyrosine kinases is also likely to be contributing to the activity of vandetanib in these tumor types; nevertheless, its relatively greater potency versus VEGFR-2 in vitro [14] suggests that vandetanib should achieve at least comparable inhibition of VEGFR-2 versus EGFR/RET in vivo. The gene discussed is EGFR; the disease is neoplasm.