Genetic mechanisms of primary resistance to EGFR inhibitors among KRAS wild-type CRC patients are represented by NRAS mutations, V600EBRAF mutations, MET amplification, ERBB2 amplification, PIK3CA mutations at the level of exon 20, mutations in FGFR1, PDGFRA, and MAP2K1, and homozygous deletions of PTEN [71]. This evidence concerns the gene EGFR and colorectal carcinoma.