Besides this, the number of resistance mechanisms to anti-EGFR therapies in CRC patients has been previously reported, including mutations of BRAF, MEK, and the EGFR extracellular domain (ECD) and the amplification of ERBB2, MET, KRAS, and NRAS, which could benefit from the inclusion of targeted therapies in standard protocols, emphasizing the importance of personalized medicine [20,21,22]. This evidence concerns the gene KRAS and colorectal carcinoma.