Moreover, ERK1/2, a downstream substrate of ERK signaling pathway, was more phosphorylated in CD4+ T cells co‐cultured with tumor‐infiltrating neutrophils and TTCS‐conditioned neutrophils than those co‐cultured with non‐tumor‐derived neutrophils and NTCS‐conditioned neutrophils, and this ERK1/2 phosphorylation was abolished when blocking B7‐H2 on tumor‐infiltrating neutrophils and TTCS‐conditioned neutrophils (Figure 6C). Here, MAPK3 is linked to neoplasm.