Considering the relevance of both the early VEGF-dependent angiogenic switch and later angiogenesis-dependent growth for BM formation in lung adenocarcinoma [3, 15, 23], these findings can best be explained by an earlier activity of the anti-VEGF/Ang2 nanobody compared to Nintedanib when it comes to interference with the brain metastatic cascade. The gene discussed is ANGPT2; the disease is lung adenocarcinoma.