Other EGFR-signaling inhibitors, such as anti-EGFR antibodies, have been approved in a subset of patients with KRAS wild-type mCRC, SCCHN and squamous NSCLC, but response rates are usually low and secondary resistance also develops through the redundancy of the EGFR signaling pathway or tumor transformation into another histologic type. This evidence concerns the gene KRAS and head and neck squamous cell carcinoma.