Amplification of the mesenchymal epithelial transition factor receptor (MET); activating mutations of downstream effectors, such as BRAF, and dual specificity mitogen-activated protein kinase kinase 1 (MEK1); oncogenic fusion with fibroblast growth factor receptor 3 (FGFR3) and CCDC6-RET; and loss-of-function mutations of phosphatase and tensin homolog (PTEN) and neurofibromin 1 (NF1) were reported to be the key elements involved in the resistance mechanisms to KRAS mutant inhibitors in lung adenocarcinoma and colorectal adenocarcinoma (56, 57). This evidence concerns the gene KRAS and lung adenocarcinoma.