For instance, we found in patients with NSCLC and EGFR mutations in the tumor tissue and prior therapy with EGFR inhibitors, secondary mutations (EGFR T790M and PIK3CA E545K) in plasma cfDNA or KRAS or BRAF mutations in the cfDNA of patients with colorectal cancer with wtKRAS in tumor tissue treated with EGFR antibodies, credibly explaining adaptive resistance to therapy. This evidence concerns the gene KRAS and neoplasm.