However, in approximately 55–60% of cases, tumor biology is characterized by mutations in the EGFR pathway (Kirsten rat sarcoma virus gene (KRAS) exons 2/3/4, Neuroblastoma RAS viral oncogene homolog (NRAS), or B rapidly accelerated fibrosarcoma gene (BRAF) genes), which lead to constitute downstream activation and primary resistance to anti-EGFR therapy, rendering EGFR inhibition an inefficient therapeutic strategy [13,14,15]. This evidence concerns the gene NRAS and neoplasm.