In hepatocellular carcinoma (HCC), CAFs promoted the activation and survival of neutrophils through the IL6/STAT3/programmed death ligand 1(PDL1) signalling pathway.78 In co‐culture with CAFs, TANs expressed more PDL1, IL‐8, CCL2 and TNF‐α.78 Neutrophils that were activated by CAFs regulated the STAT3‐PDL1 pathway to impair the immunity function of T cells in HCC.78 Zhu et al reported that neutrophils that were activated by MSCs promoted the normal transformation of MSCs into CAFs in gastric cancer with high expression of FAP, which further promoted the migration of gastric cancer cells.79 The gene discussed is CCL2; the disease is hepatocellular carcinoma.