To analyze the underlying mechanism of this induction more closely, transwell assays were performed, showing that cell‐cell contacts were needed for promoting IL‐17A‐producing Th subset polarization by tumor‐infiltrating neutrophils and TTCS‐conditioned neutrophils (Figure 6A), suggesting a surface B7‐H2, not a soluble B7‐H2 is acting in this induction of IL‐17A‐producing Th subset polarization. The gene discussed is IL17A; the disease is neoplasm.