The previous observation that EGFR is overexpressed in around 50% of patients with colorectal cancers led us to investigate the implication of EGFR in the regulation of the constitutive expression of HBD1, by testing the effect of the FDA-approved EGFR tyrosine kinase inhibitors AG1478, Afatinib, Erlotinib, Gefitinib and Osimertinib, and the anti-EGFR humanized monoclonal antibody Cetuximab interacting with the EGFR extracellular binding site to block ligand stimulation19,20. This evidence concerns the gene DEFB1 and colorectal cancer.