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). The gene discussed is MET; the disease is colorectal adenocarcinoma.