During treatment, the selective pressure induced by EGFR blockade also promotes acquired resistance, through expansion of tumor clones with mutations in KRAS18,19, EGFR (extracellular domain, ECD)3, and less frequently alterations in NRAS, BRAF, MEK1, and NF18,42 in addition to other lower prevalence alterations. This evidence concerns the gene BRAF and neoplasm.