Mutations in genes such as kirsten rats arcomaviral oncogene homolog (KRAS) and epidermal growth factor receptor (EGFR), which are prevalent in NSCLC, activate downstream effectors like phosphatidylinositol 3-Kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) and mitogen-activated protein kinase (MAPK) pathways (19). This evidence concerns the gene KRAS and non-small cell lung carcinoma.