Of note, all the patients from whom pre-treatment samples were collected and included in this analysis, experienced initial response to BRAFi/MEKi.12 Tumor specimens were evaluated for ERK signaling activity and for expression of phospho-EGFR and PDGFRβ, given their high frequency of dysregulation in glioblastoma.36 Each post-treatment sample demonstrated preserved MEK/ERK signaling at progression, along with a trend in the cohort toward increased PDGFRβ expression and EGFR activation (Figure 1A-C). The gene discussed is EGFR; the disease is neoplasm.