It is also important to note that intratumour VEGF‐A levels negatively correlate with the invasiveness of glioblastoma multiforme tumour cells44; in fact, VEGF‐A was reported as a negative regulator of receptor tyrosine kinases, by blocking their activation through direct interaction.44 These facts may account for tumour relapses during anti‐VEGF‐A therapy 44 and suggest the heterogeneity of the biological action of VEGF‐A in carcinogenesis. The gene discussed is NTRK1; the disease is neoplasm.