As a result of clonal evolution and selection [74], the ctDNA profiles of CRC patients who benefit from multiple challenging with anti-EGFR antibodies, exhibit pulsatile levels of mutant KRAS. Results revealed that the CRC genome adapts dynamically intermittent drug schedules and provided a molecular explanation for the efficacy of rechallenge therapies based on EGFR blockade [75]. Here, KRAS is linked to colorectal carcinoma.