To begin exploring the therapeutic potential of HRAS inhibition via farnesyltransferase inhibition beyond the HRAS mutant fraction of HNSCC, we reasoned that the biology of tumors driven by hyperactivity of wild-type oncoproteins is likely to resemble that of their corresponding mutant counterparts more than that of tumors with unrelated driver pathways. This evidence concerns the gene HRAS and head and neck squamous cell carcinoma.