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However, its efficacy in treating solid tumors remains limited because the immunosuppressive tumor microenvironment (ITME) seriously blocks T cell activation, infiltration, and proliferation. Cytokines, driving potent assisted function by enhanced T cell expansion, persistence, and direct tumor cell killing, have long been acknowledged as promising candidates combined with CAR\u2010T cells to improve treatment outcomes. Despite their preclinical success, significant toxicity occurs in up to one\u2010third of patients induced by powerful immune\u2010mediated cytokine release syndrome (CRS) and immune effector cell\u2010associated neurotoxicity syndrome (ICANS). In these cases, the risk\u2010benefit unbalance is less advantageous for advanced cancer therapies, appealing for a profound understanding of pathophysiological mechanisms of CRS and ICANS, as well as improved management of regulating cytokine production. 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