M1-derived EVs and their key molecule HOTTIP inhibit the progression of HNSCC by competitively binding to miR-5a-19p and miR-3b-19p to up-regulate TLR5/NF-κB signaling pathway, and M1-derived EVs and HOTTIP can polarize monocytes into anti-tumor M1 type, providing new insights into the treatment [118]. Here, HOTTIP is linked to neoplasm.