In addition, the growth of MBM cells could be more effectively inhibited in vitro if combined treatment of MAPK (BRAF) inhibitor vemurafenib and mTOR inhibitor temsirolimus.58 In EGFR‐mutated NSCLC, EGFR could induce MET phosphorylation through the RAS/ERK/p38MAPK pathway, and then enhance NSCLC invasion and even metastasis to brain.59 In summary, multi‐target combination therapy focus on tumor angiogenesis will be better for BM therapy in a manner. The gene discussed is EGFR; the disease is neoplasm.