In addition, they can be attracted to the tumor site through mechanisms dependent on CCR6/CCL20.[23] In addition, the presence of Th17 cells has been shown to inhibit proliferation and angiogenesis in HNSCC.[23] Further investigation into the mechanisms of Th17 cell differentiation and recruitment in HNSCC will help elucidate their role in promoting or inhibiting tumor progression. The gene discussed is CCL20; the disease is neoplasm.