In particular, analysis of the RAS-RAF-MAPK and phosphoinositide-3-kinase (PI3K)-AKT-mammalian target of rapamycin (mTOR) pathways responsible for modulation of tumor proliferation, migration, and angiogenesis has highlighted the presence of some somatic alterations in the NRAS, PIK3CA, and PTEN genes that could represent a potential determinant of anti-EGFR effectiveness, especially in tumors with wild-type KRAS codons 12–13. Here, EGFR is linked to neoplasm.