We have previously shown that EGFR is hyperactivated upon BRAFV600E inhibitor treatment, likely a consequence of reduced expression of the EGFR phosphatase PTPN9 upon MAPK pathway inhibition [9], and that combination EGFR and BRAF inhibition significantly improves anti-tumor efficacy in an in vivo model of BRAFV600E glioma. The gene discussed is PTPN9; the disease is neoplasm.