BRAF and melanoma: However, broader genomic analyses, looking beyond actionable variants in known genes, have the potential to inform on acquired resistance to treatments (for example, the EGFR T790M mutation confers resistance to first-generation EGFR tyrosine kinase inhibitors (TKI) in NSCLC) or to suggest potential synergistic drug combinations (for example, downstream activation of the BRAF pathway led to the combination of BRAF and MEK inhibitors in BRAF mutant melanoma) [32, 33].