SEMA7A drives breast cancer progression through pleiotropic effects, inhibition of mesenchymal factors, and promotion of macrophage-mediated lymphatic remodeling.25–28 In EGFR-mutant lung adenocarcinoma cells, SEMA7A induces EGFR-TKI resistance through ERK activation and apoptosis inhibition.29 Few studies have investigated the mechanism of SEMA7A in the initiation and progression of HNSCC. This evidence concerns the gene EGFR and head and neck squamous cell carcinoma.