For example, using molecular biopsies of focal tumor cells and cfDNA analysis to examine and monitor colorectal cancer patients, the K57T MEK1 mutation was found to be a novel mechanism of acquired resistance in patients with progressive liver metastases after long-term response to cetuximab, whereas the lesions receded with treatment of panitumumab and the MEK inhibitor trametinib and the level of the mutant MEK1 in cfDNA declined with treatment, confirming the role of cfDNA in exploring the molecular variants associated with drug resistance (Russo et al., 2016). This evidence concerns the gene MAP2K1 and neoplasm.