The most striking examples include the tyrosine kinase inhibitor treatment of EGFR-mutated pulmonary adenocarcinomas [4, 5], EGFR-directed treatment strategies in colorectal adenocarcinomas wild-type for KRAS and NRAS [6], adjuvant or neoadjuvant treatment of gastrointestinal stromal tumors carrying mutations of c-KIT or PDGFRA [7] and BRAF inhibitor treatment in BRAF V600E mutated malignant melanomas [8]. This evidence concerns the gene EGFR and colorectal adenocarcinoma.