Chimeric antigen receptor T-cell （CAR-T） immunotherapy is one of the new models of tumor targeted therapy. However，the presence of cytokine release syndrome （CRS） after CAR-T infusion is a key obstacle limiting its therapeutic effects. Macrophage activation and pyrosis of target tumor cells can trigger the release of interleukin-6 and other inflammatory factors，and excessive inflammatory factors can lead to excessive activation of endothelial cells，which is a key molecular mechanism for the escalation of CRS and the occurrence of serious adverse events. Intervention in multiple stages of cytokine production and structural optimization of chimeric antigen receptor molecules are effective strategies to reduce CRS.