A study on the mechanism of cetuximab resistance suggested that the HNSCC cell lines (OECM-1, FaDu) resistant to cetuximab upregulated the transcription factor Snail and induced direct upregulation of lymphotoxin-β and PRMT1, leading to interaction of lymphotoxin-β and methylated EGFR, and thus activated the resistance to cetuximab (32). The gene discussed is EGFR; the disease is head and neck squamous cell carcinoma.